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This technical report was developed by the American Speech-Language-Hearing Association (ASHA) Ad Hoc Committee on Apraxia of Speech in Children. The report reviews the research background that supports the ASHA position statement on Childhood Apraxia of Speech (2007). Members of the Committee were Lawrence Shriberg (chair), Christina Gildersleeve-Neumann, David Hammer, Rebecca McCauley, Shelley Velleman, and Roseanne Clausen (ex officio). Celia Hooper, ASHA vice president for professional practices in speech-language pathology (2003–2005), and Brian Shulman, ASHA vice president for professional practices in speech-language pathology (2006–2008), served as the monitoring officers. The Committee thanks Sharon Gretz, Heather Lohmeier, Rob Mullen, and Alison Scheer-Cohen, as well as the many select and widespread peer reviewers who provided insightful comments on drafts of this report.
The goal of this technical report on childhood apraxia of speech (CAS) was to assemble information about this challenging disorder that would be useful for caregivers, speech-language pathologists, and a variety of other health care professionals. Information on CAS has often been the most frequent clinical topic downloaded by visitors to ASHA's Web site. This report addresses four questions most often asked about CAS: (a) Is it a recognized clinical disorder? (b) What are its core characteristics? (c) How should it be assessed? and (d) How should it be treated?
To address these four questions, the Committee undertook a review of the scientific foundations of CAS and trends in professional practice. A preliminary survey of the literature indicated that it would not be feasible to complete a systematic review consistent with evidence-based practice. The primary barriers to such a review were unresolved controversies about the quality rankings for commonly used research designs, as proposed in several evidence-based practice systems. The Committee therefore elected to complete narrative reviews restricted to peer-reviewed literature published since 1995, with additional sources consulted as needed for coverage of certain topics. We developed a template to summarize each study and consensus procedures to evaluate the strength and quality of evidence for research findings in relation to the four questions posed above. Findings from reviews and the consensus evaluation procedures were synthesized to form the bases for the information provided in this document, including recommendations on several key professional issues. The final document incorporated extremely useful information from select and widespread reviewers who responded to invitations to review preliminary drafts of this document, including a draft posted on ASHA's Web site.
In this initial section of the report, we introduce terms and concepts, consider issues associated with the definition of CAS, and discuss scientific and professional information related to the reported increased prevalence of CAS.
The Committee recommends childhood apraxia of speech (CAS) as the classification term for this distinct type of childhood (pediatric) speech sound disorder. Beginning with the first word in this term, two considerations motivate replacing the widely used developmental with the word childhood. One consideration is that CAS support groups in the United States, the United Kingdom, and elsewhere have requested that developmental not be used in a classification term for this disorder. Inclusion of this word is reportedly interpreted by service delivery administrators as indicating that apraxia is a disorder that children “grow out of” and/or that can be serviced solely in an educational environment (see relevant discussion on the Apraxia-Kids listserv: www.apraxia-kids.org/talk/subscribe.html). A second rationale for the use of CAS as a cover term for this disorder, rather than alternative terms such as developmental apraxia of speech (DAS) or developmental verbal dyspraxia (DVD), is that our literature review indicated that apraxia of speech occurs in children in three clinical contexts. First, apraxia of speech has been associated causally with known neurological etiologies (e.g., intrauterine stroke, infections, trauma). Second, apraxia of speech occurs as a primary or secondary sign in children with complex neurobehavioral disorders (e.g., genetic, metabolic). Third, apraxia of speech not associated with any known neurological or complex neurobehavioral disorder occurs as an idiopathic neurogenic speech sound disorder. Use of the term apraxia of speech implies a shared core of speech and prosody features, regardless of time of onset, whether congenital or acquired, or specific etiology. Therefore, childhood apraxia of speech (CAS) is proposed as a unifying cover term for the study, assessment, and treatment of all presentations of apraxia of speech in childhood. As above, CAS is preferred over alternative terms for this disorder, including developmental apraxia of speech and developmental verbal dyspraxia, which have typically been used to refer only to the idiopathic presentation.
Rationales for the second and third words in the classification term CAS reflect empirical findings for children suspected to have this disorder. The alternative terms—apraxia of speech versus (verbal) dyspraxia—each have established traditions in international literatures. Apraxia of speech is more widely used in the United States following the Mayo Clinic traditions (Duffy, 2005), whereas verbal dyspraxia is the preferred term in many other English-speaking countries. Differentiating between these alternatives based solely on etymological distinction (i.e., total [a] vs. partial [dys] absence or lack of function) is problematic when applied to CAS. Clinical experience indicates that although a child suspected to have CAS may have very limited speech, seldom is a child completely without mastery of some speech sounds. Notwithstanding this difference, and to parallel usage for the possible acquired form of this disorder in adults (i.e., AOS), the Committee recommends use of the affix a for this classification term.
Several other types of apraxia and several types of dysarthria play prominent roles in the scientific foundations of CAS. Physicians and researchers recognize ideomotor and limb kinetic praxis problems that may or may not be present in persons with apraxia of speech. As discussed in this report, orofacial and limb apraxias are of particular interest as the presence of one or both in a child suspected to have CAS may provide support for the diagnosis, particularly in prelingual children. Apraxia in other systems may also play important roles in treatment. For example, the presence of limb apraxia may preclude using manual signs for functional communication. Moreover, the presence of orofacial apraxia may support the need for either more aggressive or alternative approaches to the use of phonetic placement cues in speech treatment.
Concerning dysarthria, a neuromotor disorder presumed not to involve the planning or programming deficit in apraxia (see below), some forms of these two disorders may share common speech characteristics. As discussed in later sections, a significant research challenge is to determine the diagnostic boundaries between CAS and some types of dysarthria with which it may share several speech, prosody, and voice features.
Although the core feature of CAS, by definition, is proposed to be similar to the core feature of AOS in adults, this relationship does not preclude the possibility of important differences in associated features. For example, Maassen (2002) noted that “a fundamental difference between [adult] AOS and [CAS]…is that in [CAS] a specific underlying speech motor impairment has an impact on the development of higher phonological and linguistic processing levels” (p. 263). Despite a much larger and well-developed literature in AOS, including many chapter-length discussions of alternative theoretical frameworks, the Committee elected not to include reviews of theory and research on acquired apraxia of speech in this report. This decision was motivated by the view that the scientific foundations of CAS should be based on research directly concerned with this and related childhood speech sound disorders. However, as discussed in several places in this document, the Committee has attempted to anticipate likely parallels between acquired apraxia of speech in adults and CAS, a task made more difficult by differences in terminology used to describe them. Treatment guidelines for acquired apraxia of speech have recently been proposed by the Academy of Neurological Communicative Disorders and Sciences (Wambaugh, Duffy, McNeil, Robin, & Rogers, 2006a, 2006b).
The Committee compiled a table of more than 50 definitions of CAS that have appeared in the research and clinical literature, primarily within the past 10 years. A few of the more widely cited definitions dating back to the early 1970s are provided in the table to sample the variety of perspectives on the nature of CAS among researchers, including some definitions found in secondary sources such as Web sites and professional organizations consulted by caregivers and health care professionals. We are keenly aware of the limitations of any definition of CAS until the behavioral correlates and neural substrates of this disorder have been identified and extensively cross-validated. Considering its value for children, caregivers, clinicians, researchers, and stakeholders, however, we viewed the scope of our task as including a working definition of CAS. Recognizing an almost certain need for revision based on emerging research findings, the Committee proposes the following definition:
Childhood apraxia of speech (CAS) is a neurological childhood (pediatric) speech sound disorder in which the precision and consistency of movements underlying speech are impaired in the absence of neuromuscular deficits (e.g., abnormal reflexes, abnormal tone). CAS may occur as a result of known neurological impairment, in association with complex neurobehavioral disorders of known or unknown origin, or as an idiopathic neurogenic speech sound disorder. The core impairment in planning and/or programming spatiotemporal parameters of movement sequences results in errors in speech sound production and prosody.
Review of the research literature indicates that, at present, there is no validated list of diagnostic features of CAS that differentiates this symptom complex from other types of childhood speech sound disorders, including those primarily due to phonological-level delay or neuromuscular disorder (dysarthria). Three segmental and suprasegmental features that are consistent with a deficit in the planning and programming of movements for speech have gained some consensus among investigators in apraxia of speech in children: (a) inconsistent errors on consonants and vowels in repeated productions of syllables or words, (b) lengthened and disrupted coarticulatory transitions between sounds and syllables, and (c) inappropriate prosody, especially in the realization of lexical or phrasal stress. Importantly, these features are not proposed to be the necessary and sufficient signs of CAS. These and other reported signs change in their relative frequencies of occurrence with task complexity, severity of involvement, and age. The complex of behavioral features reportedly associated with CAS places a child at increased risk for early and persistent problems in speech, expressive language, and the phonological foundations of literacy as well as the possible need for augmentative and alternative communication and assistive technology. It is useful to comment briefly on the core elements of this definition.
As required of any proposed disorder classification, definitions of CAS have three elements that may be given in any order: description of the core problem, attribution of its cause or etiology, and listing of one or more diagnostic signs or markers. Definitions of CAS, such as the one above, invariably include the proposed core problem, whereas the other two elements may or may not be addressed. One of the major differences among alternative definitions of CAS is whether the core problem is proposed to include input processing as well as production, and if so, whether auditory, sensory, and prosodic aspects of perception may prefigure in the deficit. An example of a framework that might implicate the latter is the speech motor control model in development by Guenther and colleagues (e.g., Guenther, 2006; Guenther & Perkell, 2004). Whereas some of the definitions of CAS reviewed by the Committee view the core problem as one of planning and programming the spatiotemporal properties of movement sequences underlying speech sound production, others propose that the deficit extends to representational-level segmental and/or suprasegmental units in both input processing and production.
Definitions of CAS have universally ascribed its origin to neurologic deficits, with alternative viewpoints differing with respect to specific neuroanatomic sites and circuits. There is also clear agreement that whatever the neural substrates of CAS, they differ from those underlying the several types of dysarthria. The definition of CAS proposed for this report is also clearly consistent with this neurogenic perspective.
In addition to the core problem and etiology, the third element in the proposed definition of CAS and those reviewed by the Committee is the inclusion of the key diagnostic features of the disorder. Three such features are included in the present definition, with discussion of other candidate features reviewed in subsequent sections of this report. The three features in the present definition of CAS represent a consensus conclusion based on our evaluations of the clinical research and our evaluation of comments from reviewers of preliminary drafts of this report. A major conclusion of this report is that there presently is no one validated list of diagnostic features of CAS that differentiates this disorder from other types of childhood speech sound disorders, including those apparently due to phonological-level deficits or neuromuscular disorder (dysarthria).
As with several other complex neurobehavioral disorders (e.g., autism, attention deficit hyperactivity disorder), the prevalence of CAS has reportedly increased substantially during the past decade. For example, in a study of 12,000 to 15,000 estimated diagnostic outcomes for children referred with speech delay of unknown origin from 1998 to 2004, a staff of 15 speech-language pathologists in a large metropolitan hospital diagnosed 516 (3.4%–4.3%) of these children as having suspected CAS (Delaney & Kent, 2004). Much needed population prevalence data are not available, including information by race and ethnicity. One preliminary population estimate, based solely on clinical referral data, is that CAS may occur in one to two children per thousand (Shriberg, Aram, & Kwiatkowski, 1997a), a population rate that is much lower than the rate at which this classification currently appears to be assigned. Although currently there are no epidemiologically sound estimates of the prevalence of CAS in the United States or elsewhere, several interacting factors likely contribute to clinical diagnostic figures as high as those reported by Delaney and Kent (2004).
One potential source of the apparent increased diagnostic prevalence of CAS in the past one to two decades is the impact of legislative changes during this period. Since the passage of early intervention statutes, particularly the Individuals with Disabilities Education Improvement Act of 2004 (IDEA '04, Part C), speech-language pathologists are asked to evaluate and identify communicative disorders as early as possible in infants and toddlers. A major problem in classifying young prelingual children (i.e., children with severe delays in the onset of speech) is that a diagnosis of CAS must be based on variables other than speech itself. As discussed later in this report, findings claiming that behaviors such as difficulty in feeding or excessive drooling are pathognomonic (positive signs) of CAS are tentative at best. For children suspected to have CAS who do have at least a moderate inventory of speech sounds, their communication profiles can be similar to those of children with other speech-language disorders or neurobehavioral disorders (Davis, Jakielski, & Marquardt, 1998; Davis & Velleman, 2000). Thus, although we use the term CAS for children who are the focus of the research reviewed in this document, it should be understood that the lack of a gold standard for differential diagnosis requires that all such classificatory labels be considered provisional.
Increased information on a disorder may both reflect and contribute to increased prevalence. For CAS, the past decade has seen dramatic increases in both. Interest in CAS is readily apparent when reviewing the increased number of research symposia (e.g., Shriberg & Campbell, 2003), clinical workshops, and parent support groups on CAS. Although there have been no formal accounts describing the history of this clear trend, it appears to parallel similar development in other disorders. From an academic perspective, information about CAS has traditionally been embedded within undergraduate and graduate courses in speech disorders in children or, more typically, in motor speech disorders in children and adults. However, for many speech-language pathologists, applied information on this topic is typically learned in workshops presented by persons with varying research and clinical backgrounds and/or experience with children suspected to have CAS. The Committee's anecdotal observations are that such workshops are currently among the most widely advertised opportunities for continuing education credits.
The major source of readily available information on CAS is the Internet, including its numerous Web sites and electronic discussion forums that include information on this topic. As with other unregulated medical and health-related information sources, the accuracy and usefulness of information presented on the Internet varies substantially. Some sites available internationally provide excellent information, including detailed guidelines for caregivers seeking service delivery options.
Speech-language pathologists must be knowledgeable about reimbursement alternatives and insurance guidelines. Because insurance companies frequently require that a child have a medical diagnosis to approve coverage, there may be increased use of CAS as a diagnostic classification for a severe childhood speech sound disorder. However, insurance claims for children with this diagnosis may sometimes be denied due to the continuing controversial status of CAS as a clinical entity and its increased prevalence in diagnostic coding.
Clearly the major source of overdiagnosis of CAS is the inconsistent and conflicting behavioral features purported to be diagnostic signs of CAS (Shriberg, Campbell, et al., 2003; Shriberg & McSweeny, 2002). In addition to children who may be misdiagnosed as false positives (persons said to have a disorder who do not), diagnostic guidelines also may result in false negatives (persons said not to have a disorder who do). Later discussion addresses this fundamental issue.
On the first of four questions motivating this technical report—Is CAS a clinical entity?—the Committee concludes that the weight of literature findings support the research utility of this type of speech sound disorder. A primary research source for this position is the findings on apraxia of speech that occur as sequelae to a neurological disorder and within a number of complex neurobehavioral disorders, as noted later in this document. On the second question of the core features and behavioral markers of CAS, the Committee proposes a definition of CAS that classifies it as a neurological disorder affecting the planning/programming of movement sequences for speech. However, there currently are no lists of behavioral features that are validated as necessary and sufficient for the diagnosis of CAS, although three general characteristics are proposed as possible candidates based on our narrative review and consultation with peer evaluators. On the third and fourth questions, this report does not include specific guidelines for the assessment and treatment of CAS, primarily due to the lack of research support to date for such guidelines. In a section titled Professional Issues, we review general recommendations by experienced clinical practitioners, but specific guidelines for clinical practice are deferred to future ASHA policy documents. Finally, we have noted some issues that may be associated with the recent increase in the diagnosis of suspected CAS, including birth-to-three legislation, increased availability and accessibility of information on CAS, reimbursement issues, and the lack of diagnostic guidelines.
We begin a review of the scientific foundations of CAS with an overview of typical and atypical speech acquisition, highlighting those segmental and suprasegmental behaviors that are frequently studied in CAS research. For example, we include prelinguistic speech development in each section because children suspected to have CAS are often reported to not babble at all, to babble less frequently than their typically developing peers, or to produce less mature, complex babble. Thus, a review of these foundational prelinguistic behaviors and their implications for later speech-language development seems warranted. In addition to delays in reaching developmental milestones, children suspected to have CAS may follow idiosyncratic developmental paths. For this reason, reference to typical milestones may be useful for diagnosis (i.e., atypical profiles may be suggestive of CAS).
In any discussion of speech motor control, or speech production generally, the terms variable and inconsistent are likely to arise. They are often used interchangeably and without precise definitions. This is of particular concern with respect to CAS, as some clinical investigators use inconsistency as a key classification criterion for the disorder. Some common uses of variable and inconsistent include the following:
differential use of a certain phoneme or sound class in different word positions (e.g., the child produces /k/ accurately in final position but substitutes [t] for /k/ in prevocalic position);
differential use of a certain phoneme or sound class in different word targets, even in the same word position (e.g., the child produces /m/ accurately in certain well-rehearsed words such as “mommy,” but does not produce it accurately in similar or even seemingly easier words such as “moo”);
differential use of a certain phoneme or sound class in multiple repetitions of the same word (e.g., the child produces “fish” once as “pish”, once as “pit”, once as “fit”, and another time as “shiff”). This may include measures of the number of different errors the child made in the word (e.g., in the example above, errors consisted of stopping of /f/, stopping of /∫/, and metathesis) or measures of the frequency at which a given error type is used (e.g., in the example above, stopping was the most consistent error type because stopping was used four times, and metathesis only once). This type of inconsistency is sometimes referred to as “token-to-token variability” (Seddoh et al., 1996).
Except where specified otherwise within in this document, inconsistency refers to differences in multiple productions of the same target word or syllable (i.e., token-to-token variability). Variability is used elsewhere, when meaning 1 or meaning 2, or more than one of the above meanings, is included within the findings being reported or when parameters other than speech production (e.g., pitch) are being discussed.
Beginning this review with research on typical oral-motor development, studies indicate that jaw control is established by about 15 months, before control is established for the upper and lower lips (Green, Moore, Higashikawa, & Steeve, 2000; Green, Moore, & Reilly, 2002). Motor development is slower for structures, such as the lips, that have more degrees of freedom of movement (Green et al., 2002). Tongue development is also gradual, with extrinsic tongue movements necessary for swallowing and sucking developed prior to the intrinsic tongue movements required for fine motor control (S. G. Fletcher, 1973; Kahane, 1988). Such findings are hypothesized to account for the high frequency of occurrence of infants' production of syllables that can be articulated without changes in lip or tongue configuration—including labial consonants with low and neutral vowels, coronal (alveolar and dental) consonants with high front vowels, and dorsal (velar) consonants with high back vowels (Davis & MacNeilage, 1995; MacNeilage & Davis, 1990). The high prevalence of such syllables is claimed to be associated with infants' early ability to open and close the jaw, creating the consonant-vowel alternation necessary for the syllable, with the lower lip (for labials) or the tongue (for alveolars and velars) essentially “going along for the ride.” Some clinical reports indicate that these immature patterns may persist in children suspected to have CAS (Velleman, 1994).
Through processes of differentiation and refinement, the slightly older child acquires independent control over individual articulators (lips, different portions of the tongue) and learns to produce more specialized configurations to grade movements, eventually sequencing these articulatory postures without extraneous movements (Davis & MacNeilage, 2000; Green et al., 2000). Thus, automaticity and flexibility develop over time. Both neuromotor maturation and practice are believed to underlie this developmental process, with vocal experience leading to the formation of specific neuronal pathways for finer levels of control (Green et al., 2000). Coarticulation that reflects poor temporal control or poor differentiation of structures decreases, whereas coarticulation that reflects language-specific efficiency increases, as the child becomes more adept (Nijland et al., 2002; Nijland, Maassen, van der Meulen, et al., 2003). One model of the role of perception in this process was provided by Guenther and colleagues (e.g., Guenther, 2006; Guenther & Perkell, 2004). In a following section, we will see that these developmental changes may not occur spontaneously in children suspected to have CAS.
In the present context it is especially relevant to note that mastication and deglutition (swallowing) skills are not direct precursors to speech. Motor control of feeding functions is separate from motor control for vocalization early in infancy (Moore & Ruark, 1996), as is motor control for speech breathing versus breathing at rest (Moore, Caulfield, & Green, 2001). Although “the labiomandibular movement patterns established for feeding may influence initial attempts to coordinate these structures for speech” (Green et al., 2000, p. 252), this influence is more likely to be negative than positive, as feeding patterns involve tight linking of lips with jaw in a highly rhythmic stereotyped pattern. To produce a variety of syllables within varied prosodic patterns requires the child to overcome the interdependent inflexible patterns associated with sucking. Speech requires finer levels of coordination (Green et al., 2000) but lower levels of strength than are available for other oral-motor activities (Forrest, 2002). Thus, a consensus opinion among investigators is that nonspeech oromotor therapy is not necessary or sufficient for improved speech production (see also Professional Issues: Treatment).
When children reach middle school age and even beyond, their speech production continues to be more variable, less flexible, and less accurate than adult speech. Variability is especially noted during the initial portion of speech or speech-like movements, with more feedback required for unfamiliar speech tasks (Clark, Robin, McCullagh, & Schmidt, 2001). Furthermore, as discussed in Clark et al., children's speech may be constrained by resource allocation needs, such as the need to scale back the extent of a movement in order to complete it more quickly. For example, children between the ages of 5 and 6 years are able to partially compensate for the presence of a bite block between their teeth without an increase in variability or a change in coarticulation patterns, although vowel accuracy is decreased somewhat and segment durations are increased (Nijland, Maassen, & van der Meulen, 2003). Maximum performance rates have been shown to increase with age, with changes from 3.7 same syllable repetitions of /pΛ/ per second and only 1.3 repetitions of “patty-cake” at age 2;6–2;11 [years;months] to 5.5 same syllable repetitions and 1.6 repetitions of “patty-cake” at age 6;6–6;11 (Robbins & Klee, 1987). Maximum performance rates continue to increase with maturity, with young adult same syllable repetitions typically reported at average rates between 6 and 7 per second and 5.8 to 6.9 repetitions per second of /pΛtΛkΛ/ (Baken & Orlikoff, 2000). However, Williams and Stackhouse (1998, 2000) reported that rate of speech may be a less reliable measure of motor control in preschool children than accuracy and consistency of response. Again, many of the core questions about CAS address the possibility that children suspected to have CAS have different developmental trajectories on these and other motor control parameters.
Speech development begins long before the first word is spoken. Development of this system occurs as a child gains motor control of the speech mechanism and learns the phonological rules for production of the ambient language or languages. Prelinguistic perceptual and vocal experiences lay the groundwork for later speech and language. For example, the frequency of a child's vocalizations at 3–6 months is correlated with several later developmental milestones, including performance on the Bayley Verbal Scale at 11–15 months and expressive vocabulary size at 27 months (Stoel-Gammon, 1992).
One of the most important motor precursors to first oral words is canonical babbling, the rhythmic production of repetitive consonant-vowel (CV) sequences with complete consonant closures and fully resonant vowels (Ejiri, 1998; Oller, 1986). The frequency of occurrence of “true” supraglottal nonglide consonants in babble is positively correlated with phonological development and even with language skills (Stoel-Gammon, 1992). Children who demonstrate consistent vocal motor schemes, or favorite babbles, tend to develop words earlier (McCune & Vihman, 1987). Children suspected to have CAS who are reported by their parents to have babbled very little or with very little phonetic diversity (Davis & Velleman, 2000) are at a linguistic disadvantage long before word production begins. The frequency and characteristics of early vocalizations also can be affected by perceptual factors such as early otitis media with effusion (Petinou, Schwartz, Mody, & Gravel, 1999; Rvachew, Slawinski, Williams, & Green, 1999), as well as by physiological and other factors (see Kent, 2000). Research suggests that the earliest stages of speech development in monolingual and bilingual speakers are highly similar regardless of language environment (Buhr, 1980; Davis & MacNeilage, 1995; Gonzalez, 1983; Kent, 1992; Locke & Pearson, 1992; MacNeilage & Davis, 1990; Oller & Eilers, 1982; Poulin-Dubois & Goodz, 2001; Thevenin, Eilers, Oller, & Lavoie, 1985; Zlatic, MacNeilage, Matyear, & Davis, 1997). Babbling includes stops, nasals, and glides at the labial and coronal places of articulation (Davis & MacNeilage, 1995; Kent & Bauer, 1985; Locke, 1983; Oller, Eilers, Urbano, & Cobo-Lewis, 1997), nonrounded vowels (Davis & MacNeilage, 1990; Kent & Bauer, 1985; Levitt & Aydelott-Utman, 1992), and simple CV and CVCV syllable shapes (Boysson-Bardies, Sagart, & Bacri, 1981; Buhr, 1980; Oller & Eilers, 1982; Vihman, Ferguson, & Elbert, 1986).
In the first linguistic stage, from 12 to 18 months, babbling decreases and word production increases. While slight differences in frequencies of sounds and word shapes are reported cross-linguistically (Boysson-Bardies & Vihman, 1991; Maneva & Genesee, 2002), the considerable cross-linguistic similarities observed in babbling also exist in first words. Children from various language environments mainly produce coronal and labial stops, nasals, and glides, and simple CV syllable shapes in their first words (Boysson-Bardies & Vihman, 1991; Eilers, Oller, & Benito-García, 1984; Gildersleeve-Neumann, 2001; Goldstein & Cintrón, 2001; Oller, Wieman, Doyle, & Ross, 1976; Teixeira & Davis, 2002; Vihman et al., 1986). In addition, limited research on English-learning infants and infants in other monolingual language environments suggests that low front, non-rounded vowels are most frequent in first words (Davis & MacNeilage, 1990; Gildersleeve-Neumann, 2001; Levitt & Aydelott-Utman, 1992; So & Dodd, 1995; Stoel-Gammon & Dunn, 1985; Teixeira & Davis, 2002). Research on sounds in the first words of simultaneous bilinguals is extremely limited; however, it appears that similar consonants (Keshavarz & Ingram, 2002) and word shapes (Kehoe & Lleo, 2003) predominate. Information is not currently available on possible cross-dialectal differences.
Children's early speech patterns include phonotactic errors such as reduplication (e.g., “wawa” for “water”), consonant harmony (e.g., “goggie” for “doggie”), and final consonant deletion (e.g., “da” for “dog”) during their first 12–18 months of word production; these error patterns typically are markedly diminished by 3 years of age in children who are typically developing, although not, as reviewed later, in children suspected to have CAS. Apparent regression, in which the child produces a word less accurately but also with less variability than before, may also occur during the first year of word production as children systematize their phonologies (Vihman & Velleman, 1989). Individual sounds may be produced variably, even within the same word, although speech production patterns (i.e., frequent phonological processes) are consistent (Demuth, 2001; Ferguson & Farwell, 1975; Taelman & Gillis, 2002; Velleman & Vihman, 2002).
Between the ages of 2 and 3 years, the speech sound system of typically developing children expands in complexity, resulting in productions of a greater variety of consonants, vowels/diphthongs, and word shapes. By this age, children in English-learning environments begin to produce the more complex sounds—velars, fricatives, affricates, and liquids—generally mastering the majority of sounds with these features by approximately 5 years of age (Stoel-Gammon & Dunn, 1985). The few studies that have examined vowel and diphthong development suggest that accurate production of all vowels and most diphthongs (but not rhotic vowels) is achieved by age 3 (Bassi, 1983; Larkins, 1983; Pollock & Berni, 2003). In Pollock and Berni's study, the average percentage of vowels correct for children between 18 and 23 months was 82%, increasing to 92% for 24- to 29-month-olds, 94% for 30- to 35-month-olds, and 97% by 36 months of age. As subsequently discussed, the picture is very different for children suspected to have CAS. For typically developing children, more complex word shapes become frequent during this early period, with many consonant clusters, final consonants, and unstressed syllables correctly produced, resulting in a large increase in accuracy and intelligibility (Stoel-Gammon & Dunn, 1985). Consonant clusters emerge by the first third of the fourth year (36–40 months), usually appearing first in final position in speakers of Mainstream American English (Kirk & Demuth, 2003). Typically developing children are reportedly 26%–50% intelligible by 2 years, 71%–80% intelligible by 3 years, and 100% intelligible by 4 years (Coplan & Gleason, 1988; Weiss, 1982). It is also after age 2 that the diverse effects of a child's ambient language become most apparent (see below; Goldstein & Washington, 2001; Johnson & Wilson, 2002; Walters, 2000).
In typical and most atypical, nonapraxic speech during this age period, earlier developing sounds tend to be substituted for later developing sounds that the child may not be able to produce as easily (e.g., stops substitute for fricatives and glides substitute for liquids). Children with nonapraxic speech sound disorders appear to be most successful at producing the correct voicing features of a segment and least successful at maintaining the correct place of articulation (Forrest & Morrisette, 1999). Although perceptual and articulatory constraints are the primary posited source of English-learning children's difficulty with affricates, fricatives, and liquids, the frequency of sounds in a particular environment also plays an important role in the age and order of phoneme mastery. Children from language environments with a greater frequency of occurrence of certain less universally common sounds (e.g., liquids, fricatives) tend to produce these sounds earlier and better, suggesting the early influence of the ambient language. For example, Russian children who are exposed to many palatalized consonants as well as non-palatalized consonants typically master the palatalized ones first (Zharkova, 2004). Other research in non-English monolingual language environments has shown ambient language effects on the greater earlier accuracy of fricatives and affricates (Pye, Ingram, & List, 1987) as well as dorsal sounds and multisyllabic words (Gildersleeve-Neumann, 2001; Teixeira & Davis, 2002). In addition, children in other language environments may produce words with different error patterns. For instance, it is common for young Finnish children to have initial consonant deletions, an atypical phonological process in English-speech acquisition (Vihman & Velleman, 2000).
Ambient language effects on speech sound acquisition are also observed in bilingual children. Bilingual children may show an effect of each language on their productions within that language, such as reported for a Hindi-English simultaneous bilingual child who used predominantly monosyllables in English and predominantly disyllables in Hindi (Bhaya Nair, 1991; Vihman & Croft, in press).
Simultaneously bilingual children produce different segments and word shapes depending on which of their two language environments they are in (Holm & Dodd, 1999; Holm, Dodd, Stow, & Pert, 1999; Johnson & Lancaster, 1998; Kehoe & Lleo, 2003; Keshavarz & Ingram, 2002). Mixing of errors has been observed in the carryover of the phonetic and phonological properties of one language to the other, resulting in greater rates of error when compared to monolingual peers (Goldstein & Cintrón, 2001). Although bilingual children may follow the general developmental path, their speech patterns might still be expected to be influenced by the phonology/ies of their native language(s). Clearly, the large, cross-linguistic literature on typical and atypical speech sound acquisition provides a rich database for comparative research on speech development in children suspected to have CAS.
Infants' early discrimination of prosody (see Speech Perception) is followed by production of language-specific prosodic patterns. By 6–12 months, their vocalization patterns reflect the dominant prosodic contours (e.g., falling vs. rising pitch; Whalen, Levitt, & Wang, 1991) of the ambient language.
English-speaking children use falling intonation contours first, then rising contours, to mark phrase and utterance boundaries (Tonkava-Yampolskaya, 1973). Typical English-learning children have been shown to use frequency, amplitude, and duration appropriately to mark sentential emphasis (Skinder, Strand, & Mignerey, 1999), as do children with speech delays (Shriberg, Aram, & Kwiatkowski, 1997b, 1997c). The primary period for the development of prosody occurs from approximately 5 to 8 years of age (Local, 1980; Wells, Peppe, & Goulandris, 2004). However, even typically developing children may not have adultlike comprehension and production of prosody until 10 or 12 years of age (Allen & Hawkins, 1980; Morton & Trehub, 2001). In English, later-developing prosodic functions include the production of compound words, rise-fall or fall-rise prosody on a single word to convey emotion, high rising pitch to request clarification, accent on a nonfinal word to convey emphasis (e.g., “I want a black bus”), and the comprehension of another person's use of accent to emphasize a certain part of an utterance (Wells et al., 2004).
Children's stress patterns parallel the dominant stress patterns of their languages in late babbling and early words (e.g., predominantly trochaic stress-first patterns in English; iambic stress-last patterns in French; Vihman, DePaolis, & Davis, 1998). By 2½ years of age, English learners' vowel durations differ appropriately in stressed versus unstressed syllables (Smith, 1978), and they are able to produce weak syllables in initial position (e.g., the first syllable of “giraffe”) and between two stressed syllables (e.g., the second syllable of “telephone”; Gerken, 1994; Kehoe & Stoel-Gammon, 1997). Children with speech delay but not apraxia cease to delete such weak syllables by age 6 (Velleman & Shriberg, 1999); as reviewed later, children suspected to have CAS may persist in such patterns. By age 6, typically developing children have different coarticulatory and temporal patterns depending on the syllable structure of a word. For example, Dutch-learning children have coarticulation and duration patterns that differ with the metrical structure of the word (Maassen, Nijland, & van der Meulen, 2001; Nijland, Maassen, van der Meulen, et al., 2003).
Between birth and 2 months of age, human beings are already able to discriminate among languages with different rhythmic patterns (Mehler et al., 1988), among words that differ by number of syllables (Bijelac-Babic, Bertoncini, & Mehler, 1993), and among different vowels (Kuhl & Miller, 1975) and different consonants (Eilers, 1977; Eilers & Minifie, 1975; Jusczyk, Murray, & Bayly, 1979; Levitt, Jusczyk, Murray, & Carden, 1988). Some of these capacities may be innate, but others are learned through perceptual experience. For example, the neonate attends longer to her own mother's voice (DeCasper & Fifer, 1980) and to her own language prosody in conversational speech (Mehler et al., 1988). Speech perception skills become more and more language-specific as the child approaches 1 year of age. By 10 months, infants display preferences for stress patterns (Jusczyk, Cutler, & Redanz, 1993; Morgan, 1996; Weissenborn, Hohle, Bartels, Herold, & Hofmann, 2002), consonants, and sequences of consonants and vowels from their own language (Gerken & Zamuner, 2004; Jusczyk, Friederici, Wessels, Svenkerud, & Jusczyk, 1993; Jusczyk, Luce, & Charles-Luce, 1994). Furthermore, at 10–12 months, babies are less able than at earlier ages to discriminate segmental contrasts that are not relevant to their own languages (Werker & Tees, 1984).
At 4 years of age, children with nonapraxic speech disorders are significantly worse than their typically speaking peers at discriminating commonly misarticulated sounds from sounds that are generally substituted for them. There is a significant difference between the two groups' ability to identify whether a sound was produced correctly versus incorrectly within a word (e.g., [tæt] vs. [kæt] for “cat”) (Rvachew, Ohberg, Grawberg, & Heyding, 2003).
Children with speech delay often also have language delays, especially in expressive morphology (Paul & Shriberg, 1982; Rvachew, Gaines, Cloutier, & Blanchet, 2005). Their morphological errors cannot be attributed to speech difficulty. For example, Rvachew et al. reported that children with speech delay omitted /s/ and /z/ in final position more often in grammatical morphemes (plural, third person singular) than in uninflected words even though the phonetic complexity was the same in both contexts. Furthermore, frequency of omission of morphemes was correlated with mean length of utterance ([MLU] in words), not with articulatory skills.
A few studies have investigated profiles of children with speech delay only versus those who also have language delay. In a study of 15 children with speech delay only and 14 children with both speech and language delay, Lewis, Freebairn, Hansen, Iyengar, and Taylor (2004) reported that the speech patterns of the two groups were similar at school age (ages 8–10 years), with frequent liquid simplifications and distortion errors. The speech delay only group persisted in immature consonant harmony/assimilation errors, whereas the speech and language delay group produced frequent final consonant deletions, which, although not described in this study, may have been associated with morphological deficits. As part of a larger study, Nathan, Stackhouse, Goulandris, and Snowling (2004) followed 19 children with speech delay only and 19 children with both speech and language delay from preschool (age 4;6) through kindergarten (age 5;8) to school age (age 6;9). In preschool, the speech delayed only group performed better overall on articulation assessments as well as on language measures. At the two later ages, the children with speech delay only seemed to have normalized (caught up to typically developing peers), whereas the deficits of the speech and language delay group persisted. To date, there are no studies that have systematically compared specific language patterns (e.g., morphological vs. syntactic errors) in children with language delay only to those of children with both speech and language delay.
Studies indicate that at age 4, children with speech delay are at higher risk for impaired phonological awareness skills (e.g., rhyme matching, onset segmentation, onset matching) compared to children who are typically developing, although in one such study significant differences between the two groups' early literacy skills were not detected (Rvachew et al., 2003). Between the ages of 6 and 8 years of age, children without speech sound or language disorders develop the metalinguistic ability to explicitly identify the number of syllables in a word and the placement of individual sounds or clusters within words (Marquardt, Sussman, Snow, & Jacks, 2002). Children with a familial history of speech delay/disorder (including those with CAS, as discussed in the following section) are at higher risk for literacy difficulties, especially if they also demonstrate language delay (Bird, Bishop, & Freeman, 1995; Larrivee & Catts, 1999; Lewis et al., 2004; Nathan et al., 2004; Webster & Plante, 1992). In a study of 47 children with speech deficits only (reportedly including CAS), speech and language deficits, or no speech or language deficits, Nathan et al. reported that preschool language ability, especially for expressive language, is a strong predictor of later phonemic awareness skills. These investigators also found that persistent speech difficulties (beyond age 6;9) are strongly predicted by concurrent deficits in phonemic awareness. An ASHA document (ASHA, 2001) includes useful information about phonological awareness development and disorders.
The large literature on typically developing speech has been reviewed from the perspective of the key areas of possible developmental differences between children who are typically developing, children with nonapraxic speech sound disorders, and children diagnosed with CAS. The goal was to provide a reference basis for the review of CAS literature to follow. Notable areas of difference were found in the early and seemingly effortless development of vowels and prosody in children who do not have CAS. Important areas of overlap in the speech of typical learners and children suspected to have CAS include the gradual development of consonant repertoires and phonotactic structures (syllable and word shapes) and gradual decreases in both variability and inconsistency. Research indicates that children with any type of speech sound disorder are at increased risk for language and literacy difficulties, although the literature reviewed in the next section indicates that children suspected to have CAS may be at considerably greater risk.
Studies of the developmental neurobiology of CAS are expected to provide an understanding of the relevant neural substrates and identify useful early diagnostic biomarkers. Even when such information becomes available, speech-language pathologists will still need to use behavioral tools (e.g., standardized tests, informal assessment measures, parental observations, reports from other professionals) to provide the individualized profiles needed to differentiate children suspected to have CAS from children with other types of speech-language disorders. To date, as previewed in the Introduction and Overview, no one test score or behavioral characteristic has been validated to differentially diagnose CAS (i.e., there are no necessary and sufficient markers). The present section provides an extended review of behavioral research in CAS.
In both research and clinical settings, the diagnostic challenge is to differentiate CAS from speech delay, dysarthria, and other speech sound disorders. Many of the speech and other behaviors (i.e., signs) thought to be associated with CAS are also found in children with more broadly defined speech sound disorders (McCabe, Rosenthal, & McLeod, 1998). The differentiation between apraxia and dysfluency (stuttering, cluttering) is a less common clinical need, although there are some behavioral overlaps and children suspected to have CAS may go through periods of dysfluency (Byrd & Cooper, 1989). The question of differentiating language behaviors occurring in CAS from those in specific language impairment (SLI) is also highly challenging, a question that has only recently begun to be addressed in the clinical literature (Lewis et al., 2004).
Behavioral variables that have been studied in association with CAS can be divided into six major domains: nonspeech motor, speech production, prosody, speech perception, language, and metalinguistic/literacy. Within each of these domains, reference is made to core deficits in timing, programming, and sensorimotor coordination. However, due to the lack of a definitive diagnostic marker for CAS, conclusions from studies seeking to identify such markers are limited by issues of participant selection and circularity. When study participants are selected based solely on clinician referrals, it is difficult to determine which diagnostic criteria were used by individual clinicians, how clinicians differentially weighted their criteria, and the amount of agreement within and between clinicians. In fact, clinical agreement has not been demonstrated in recent studies. Davis et al. (1998) and Forrest (2003) reported high degrees of clinical disagreement among practicing speech-language pathologists in their criteria for diagnosing CAS. There are similar problems in research contexts. In a recent CAS study, two research teams were able to reach only 55% agreement on the assignment of 35 speech sound disordered study participants to CAS or non-CAS groups (Shriberg, Campbell, et al., 2003). This diagnostic uncertainty among both clinicians and researchers is the primary barrier to research on the underlying nature of CAS. As suggested by Strand (2001), another significant research constraint is the heterogeneity of children with CAS due to the co-occurrence of other disorders with CAS, as well as individual differences in compensatory behaviors that may be secondary to the primary deficits.
Definitional circularity is most evident when study participants are selected based on the presence of certain signs and those signs or derivatives of them are part of the study's descriptive findings. Because of the presumed low prevalence of CAS, it is difficult to conduct large scale studies of children with etiologically undifferentiated speech sound disorders hoping to identify speech and other characteristics unique to CAS. Moreover, there is increasing evidence that the signs of CAS not only vary among children with the disorder, but also change as children mature (Lewis et al., 2004; Shriberg, Campbell, et al., 2003). Thus, although there may be neural phenotypes that persist beyond the developmental period, it is likely that behavioral markers will need to be developed for several developmental epochs. CAS may be a complex of signs, with varying neurologic, motor, and behavioral characteristics that can be identified only by its unique profile over time (Ekelman & Aram, 1983). It is vital not to confuse descriptions with explanations; the varying behavioral consequences of a disorder can obscure as well as clarify its fundamental nature. Within each of the six behavioral domains listed above, we report findings supporting associations with CAS, followed by some perspectives on theories of CAS.
Nonspeech motor behaviors are primarily used to differentiate children suspected to have CAS from children with various types of dysarthria, although there is some overlap between the two motor speech disorders. Nonspeech motor signs of CAS that are most commonly proposed in the literature (some of which are also cited as signs of dysarthria) include the following: general awkwardness or clumsiness, impaired volitional oral movements, mild delays in motor development, mildly low muscle tone, abnormal orosensory perception (hyper- or hyposensitivity in the oral area), and oral apraxia (e.g., Davis et al., 1998; McCabe et al., 1998; Shriberg et al., 1997a). The nonspeech motor features typically listed for oral apraxia are impaired volitional oral movements (imitated or elicited postures or sequences such as “smile-kiss”) and groping (e.g., Davis et al., 1998; McCabe et al., 1998; Shriberg et al., 1997a). Murdoch, Attard, Ozanne, and Stokes (1995) documented weaker lingual muscles and reduced tongue endurance in children who demonstrated oral apraxia than in typically developing children; a nonapraxic, phonologically disordered control group was not included in the study. Dewey, Roy, Square-Storer, and Hayden (1988) found that limb, oral, and verbal apraxia tend to co-occur in children. They highlighted the transition difficulties (moving from one action in a sequence to the next) exhibited by children “with a specific deficit in verbal sequences of consonantvowel syllables” (p. 743) and noted that repetition of the same action was far less of a problem. They also stressed the volitional aspect of the disorder, as did Maassen, Groenen, and Crul (2003) and D. Nelson (1995). Specifically, Dewey et al. (1988) found that demonstrating the action of an object was a problem for their participants with CAS only when the children were miming the action without the object in hand. Crary and Anderson (1991) also noted that compared to children without a diagnosis of CAS, children with this diagnosis had slower rates and less accurate performance on sequences of hand and facial movements.
Motoric aspects of speech, especially repetitions of syllables (maximum repetition rate [MRR]) and productions of alternating syllables (diadochokinesis [DDK] or alternating motion rate [AMR]), are commonly used to diagnose CAS both clinically and for research participant selection. The utility of these measures has been verified in several research studies, including Davis et al. (1998), McCabe et al. (1998), Nijland et al. (2002), Thoonen, Maassen, Gabreëls, and Schreuder (1999), and Thoonen, Maassen, Wit, Gabreëls, and Schreuder (1996). Thoonen et al. (1996), for example, reported that maximum sound prolongation of vowels (e.g., producing /a/ for as long as possible) and MRRs for single syllables (e.g., /pΛtΛkΛ/ etc.) differentiated children with a diagnosis of spastic dysarthria from both children with a CAS diagnosis and those who were typically developing. Maximum sound prolongation of fricatives and maximum repetition rate of trisyllabic sequences (/pΛtΛkΛ/) differentiated children with apraxia from those who were typically developing. Thus, the differences between children with CAS and those who were typically developing were only significant for the more complex tasks (prolongations of more difficult consonant sounds; sequences of different syllables). Control groups of children with other speech sound disorders of unknown origin were not tested. Lewis et al. (2004) found significant differences between preschool and school-age children with CAS and matched children with non-CAS speech delay in their ability to repeat nonwords and multisyllabic words, with the CAS group performing more poorly. Children with CAS also had significantly lower Total Function scores on the Robbins and Klee (1987) oral-motor assessment, which includes DDK. Moreover, children with CAS had more difficulty on the Fletcher Time-by-Count test of DDK (S. G. Fletcher, 1978) at school age.
Lists of the speech behaviors proposed to characterize CAS abound in the research and clinical literatures. Frequent characteristics include some features that clearly are shared with other speech sound disorders (McCabe et al., 1998), including slow development of speech, reduced phonetic or phonemic inventories, multiple speech sound errors, reduced percentage of consonants correct, and unintelligibility. Commonly proposed characteristics (Davis et al., 1998; McCabe et al., 1998; Shriberg et al., 1997a) that are less likely to be found in children with nonapraxic speech sound disorders include reduced vowel inventory, vowel errors, inconsistency of errors, increased errors in longer or more complex syllable and word shapes (especially omissions, particularly in word-initial position), groping, unusual errors that “defy process analysis,” persistent or frequent regression (e.g., loss of words or sounds that were previously mastered), differences in performance of automatic (overlearned) versus volitional (spontaneous or elicited) activities, with volitional activities more affected, and errors in the ordering of sounds (migration and metathesis), syllables, morphemes, or even words. However, many of these features are found in children who do not fit the overall pattern of CAS (McCabe et al., 1998), leading some reviewers to question their diagnostic specificity for CAS (e.g., Macaluso-Haynes, 1978). Moreover, as discussed later, many of these posited features are not consistent with a deficit in praxis. For example, motor speech theories typically assign selection and sequencing of sounds, syllables, and words to a processing stage that precedes the planning and programming of movements needed to realize these units as manifest speech. Error patterns that are not consistent with a praxis deficit but are especially common in children suspected to have CAS need to be studied to understand whether or not they are causally related and, if they are, to identify the explanatory mechanisms.
Detailed studies of differences between children suspected to have CAS compared to those with typical development or with other subtypes of speech delay have sought to identify the diagnostic characteristics of CAS. As noted previously, all such studies have research design limitations due to the lack of certainty that the children suspected to have CAS indeed have this disorder. As just one of many examples, Maassen et al. (2001) reported that children with CAS have less predictable speech errors than children who are typically developing. These authors provided useful acoustic data documenting a lack of systematic effects of given phonetic contexts on certain sounds in the speech production of children with CAS. However, because of the absence of a control group of children with other speech sound disorders and because the only inclusionary criterion information provided was that “Clear cases of [CAS] were selected according to clinical criteria described by Hall, Jordan, and Robin (1993) and Thoonen et al. (1996)” (Maassen et al., 2001, p. 146), it is difficult to evaluate claims that variability of this type may be a unique feature of CAS.
Speech sampling methods may also be crucial to interpretation of findings. Shriberg et al. (1997b) reported that a group of children, chosen by five individual researchers as exemplars of these researchers' diagnosis of CAS, did not have any speech production errors in conversational speech that could be used to differentiate them from control children with speech delay of unknown origin. A potential constraint on these findings, as discussed more recently in Shriberg, Campbell, et al. (2003), is that these findings were based on conversational speech samples, rather than on children's responses to challenging speech production tasks designed to evoke more discriminative error patterns.
In a widely cited study of speech motor behaviors, McCabe et al. (1998) attempted to identify potential features of apraxia retrospectively (from clinic files) in a mixed group of 50 children with speech disorders, 9 of whom had been identified as having apraxia of speech by their speech-language pathologists. They described characteristics of CAS in some of the 50 children who had been classified as speech disordered (non-CAS). The characteristics most often identified in the total group were “changed level of awareness of own speech errors, problems with imitation of speech, breathing difficulties/asthma/allergies, decreased performance on DDK tasks, and presence of ‘soft’ neurological signs or minimal brain damage” (McCabe et al., 1998, p. 113). These were also the most commonly reported symptoms in the subset of children who previously had been identified by their speech-language pathologists as having apraxia. However, McCabe et al. reported “inconsistent speech performance,” vowel errors, and incorrect production of “lingual phonemes” (/l/, /r/) as best differentiating this CAS group from their other participants. Other differences that distinguished the two groups quantitatively included slow development of speech, idiosyncratic sound substitutions, and syllable omissions.
Lewis et al. (2004) compared a group of children suspected to have CAS to two other groups of children longitudinally: one group with non-CAS speech sound disorders only and one group with both speech and language disorders. The CAS group was selected based on both a diagnosis of CAS by the child's speech-language pathologist and on the child meeting at least four out of eight criteria for CAS. The CAS group differed from the speech disorder group, especially at school age, on syllable structures, sound sequencing, vowel and voicing errors, unusual types of errors, and the persistence of their error patterns. At school age, the children with CAS had more speech errors overall, more unusual errors, and more syllable sequencing errors in conversational speech than the children with both speech and language disorders (but see McNeil, Robin, & Schmidt, 1997, for an alternative interpretation of phoneme-level sequencing errors in AOS).
Ball, Bernthal, and Beukelman (2002) used a very careful procedure to identify participants with CAS, including diagnosis by a speech-language pathologist and administration of the Screening Test for Developmental Apraxia of Speech (Blakeley, 1980) and the Tasks for Assessing Motor Speech Programming Capacity (Wertz, LaPointe, & Rosenbeck, 1984). A panel of three speech-language pathologists then rated each child on a scale of 1 (not CAS) to 5 (definitely CAS) based on a list of 17 characteristics of CAS. The 36 children included in the study each had an average rating of at least 3. They also had other co-occurring language, social, and behavioral impairments. The purpose of the study was to attempt to identify more inclusive communication profiles of children with CAS. Following this identification procedure, an assessment battery of tests and measures was administered to the participants, and test results were subjected to cluster analysis to identify groups of participants who shared particular patterns of communication performance. Twelve of the participants who had been rated as having a high likelihood/severity of CAS had notable deficits in the following areas compared to participants in the other clusters: receptive language, vocabulary, MLU, percentage of consonants correct, intelligibility, and behavior.
Acoustic analyses have been used by several authors to characterize more precisely the speech production differences of children with CAS. Participants with CAS in these studies have demonstrated decreased differentiation of stop place of articulation (Sussman, Marquardt, & Doyle, 2000), decreased differentiation of vowels (Nijland et al., 2002), higher degrees of anticipatory coarticulation within syllables (Maassen et al., 2001; Nijland, Maassen, van der Meulen, et al., 2003), lack of impact of syllable boundaries or syllable shape on coarticulation (Maassen et al., 2001; Nijland, Maassen, van der Meulen, et al., 2003), lack of intersyllabic coarticulation, and variable idiosyncratic patterns (Nijland et al., 2002) that were less predictable acoustically in any given phonetic context (Maassen et al., 2001). Nijland, Maassen, van der Meulen, et al. (2003) further noted that children with CAS had higher scores than typically developing children on measures of coarticulation and vowel accuracy when a bite block was placed between their teeth. As noted previously, additional studies using control groups of children with other forms of speech delay would strengthen the claims of this carefully executed study series.
With respect to severity, McCabe et al. (