Defining Developmental Apraxia of Speech - Case Study Example

Defining Developmental Apraxia of Speech and differentiating it from Acquired Apraxia of Speech in APA Style Defining Developmental Apraxia of Speech and differentiating it from Acquired Apraxia of Speech Introduction Apraxia of speech is a disorder, in which the person has difficulty in speaking clearly and consistently. Shipley and McAfee define it as “a neurologically based motor speech disorder that adversely affects the abilities to execute purposeful speech movements” (as cited in Tobin, 1997, p. 216). Developmental and Acquired Apraxia of Speech (DAS and AOS) are two types of apraxia. The purpose of this essay is to define developmental apraxia of speech, examine the issues and various perspectives surrounding its existence, its diagnosis and to compare and contrast it to acquired apraxia of speech. Developmental Apraxia of Speech: Definition, Diagnosis and Theoretical Perspectives Given the nature of this disorder, it is difficult to define it. Guyette and Diedrich doubt it is possible to define DAS in the normal sense as “there is little reported agreement on which symptoms the behaviors are important in the diagnosis of this disorder. Second, there is paucity of data to support claims even when agreement is found” (as cited in Bishop & Rosenbloom, 1987, p. 30). This view notwithstanding, various definitions have been propounded for DAS. Hegde (2001) states that it is a “disorder in children characterized by sensorimotor problems in positioning and sequentially moving muscles for the volitional production of speech, associated with prosodic problems” (p. 184). Caruso and Strand (1999), state that most definitions of developmental apraxia of speech “focus on the inability or difficulty with the ability to perform purposeful voluntary movements for speech, in the absence of paralysis or weakness of the speech musculature” (p. 14). Despite lack of evidence and consensus regarding the symptoms and characteristic features of DAS, certain diagnostic symptoms have generally been agreed upon. “These comprise a high number of consonant errors, especially substitution in place of articulation, inconsistency in repeated productions, difficulty in sequencing phonemes, especially in diadochokinetic tasks (/pataka/), groping, and resistance to therapy” (Nijland & Maassen, 2005, p. 138). Other diagnostic criteria include errors in articulation, use of vowels, lack of comprehensive skills, faulty sequencing and rhythm of speech. However it cannot be said with any degree of certainty that these symptoms are exclusive to DAS. Shriberg, Aram and Kwiatkowski (1997b) attempted to find one diagnostic marker that was exclusive to DAS and that served to differentiate it from children with delayed speech and found “inappropriate stress the only characteristic significantly differentiating the two groups” (p.307). Unfortunately the study was not entirely conclusive as about 48% of children with suspected DAS did not show inadequate stress patterns. Shriberg et al., (1997c) have countered this shortcoming by suggesting that inappropriate stress is “a diagnostic marker for one or at least two subtypes of DAS, with the other subtypes(s) requiring some other diagnostic marker(s)” (p. 324). This is a convincing argument. But the methodology used by Shriberg et al., have been questioned by Kent who “noted that perceptual judgments for voice and speech are limited in several areas such as nonequivalent definitions, low consensus, and poor reliability among listeners” (as cited in Munson, Bjorum, & Windsor, 2003, p. 190). Studies have found that children with DAS are inconsistent in their speech. But this is not a reliable diagnostic marker. Like most disorders, symptoms of DAS range from mild to severe. However, in many instances children with severe speech disorder that is of lengthy duration are diagnosed with DAS. According to Bahr, Velleman and Ziegler (1999), “In many clinical settings, DAS appears to be a diagnosis of last resort; that is, if the child’s phonology is severely impaired and he or she does not improve with treatment, it must be DAS” (p.21). Another telling feature is that these children do not respond to speech therapy or treatment procedures favorably. Hall, Jordan and Robin, state that DAS is resistant to “traditional or conventional remediation techniques” (as sited in Forrest & Marrisette, 1999, p. 187). A diagnosis of DAS is also given after a process of due elimination, in which the possibility of other speech disorders are ruled out. The conceptual approaches to DAS include motor, speech development and cognitive perspectives. Maassen (2002) describes speech development “as a complex progress that depends on the timely interplay of perceptual, motor, and higher cognitive functions” (p. 262). According to the speech production model there are five stages involved in the production of speech – phonological encoding, mental syllabary, phonetic planning, motor programming and motor execution (as cited in Nijland & Maassen, 2005). Errors in one of these levels may impact the functioning of the other levels as the sequential development of speech is thrown out of joint. In phonological encoding the words necessary for speech are determined and a phonological plan is formulated, regarding its exact usage. Any defects at this stage result in the disruption of the articulation schema and interfere with normal speech development. Mental syllabary “is a repository of gestural programs of frequently used syllables that are collected during phonetic planning” (as cited in Nijland & Maassen, 2005, p. 140). Malfunctioning in this area results in hesitation, prolonged pauses, and a lack of continuity and coherence. Phonetic planning involves the development of a phonetic plan. Defects in this level manifest themselves in the retrieval of phonetic plans and results in groping. It also affects spontaneity in speech as opposed to mechanical or standard responses. In the case of the former kind of speech, the context in which speech is used has bearing, while the latter type of speech is cognitive in nature or learned. At the motor programming level instructions are formulated in keeping with the phonetic plan. Deficits at this level result “in problems such as sound distortions, voicing errors, resonance inconsistencies, or phonetic variability of production” (Nijland & Maassen, 2005, p. 141). Finally in the motor execution stage, the muscles involved in speech are brought into play. Defects in this stage are largely pathophysiological. Errors occurring at one or more levels of speech production may herald the onset of DAS, but opinions are diverse and favor linguistic, motor or cognitive approaches or a combination of all three. The articulatory movements that are required to carry out the phonetic plan are determined in the motor programming level and are susceptible to physical limitations as well as contextual and environmental factors. Lip movements come into play in producing the required consonants or vowels. If there is a discrepancy between the child’s physical ability and language and cognitive skills, there is impairment of speech and causes can be traced directly to motor causes. Ordinarily people can compensate and produce legible speech even while the lips are otherwise occupied for instance while sucking on a sweet. Studies on compensation abilities using a “bite block” were done on normal children and those with suspected DAS. These studies have yielded mixed results. However, Nijland, Maassen and van der Meulen (2003) have provided evidence to support their hypothesis that defects in motor programming are found in children with DAS, “findings on the speech production of the children with DAS investigated in the present study are indeed indicative of a problem at the level of motor programming” (p. 448). There are those who reject the motor programming approach and embrace a linguistic perspective in order to explain DAS. According to Shriberg et al., (1997a) “there are several research groups who emphasize that unlike children with some other motor speech disorders, children with suspected DAS invariably have language deficits”(p. 277). Velleman and Strand propose, “phonologically based deficits in representation” (as cited in Davis, 2003, p.122) as the underlying deficit in DAS. Adherents to this theory believe that phonological representation is impaired in children with suspected DAS. Therefore they are unable to fall back on their memory and learned vocabulary to retrieve the needed lexemes or word forms or to formulate a phonological plan that is a prerequisite for motor programming and execution. Thelen and Smith meanwhile point out “The interaction between cognitive processes, motor activities and learning” (as cited in Forrest & Marrisette, 1999, p. 187), which may explain the complex etiology of DAS. Differentiating Acquired Apraxia from Developmental Apraxia of Speech Similar to DAS, defining AOS poses a problem, as a number of factors complicate the issue. McNeil states that “it is the lack of a definition and an agreed – upon set of criteria for subject selection that is the single most important impediment to theoretical and clinical advancement” (as cited in Maassen, 2002, p. 263). Therefore like in DAS, there is no conclusive underlying factor or a concrete criterion of symptoms that is needed for a differential diagnosis. Acquired apraxia of speech (AOS) is “A neurogenic speech disorder with documented neuropathology in the left cerebral hemisphere…” (Hegde,2001, p.57). It is this evidence of underlying neuropathology that serves to distinguish AOS from DAS. The neurogenic factor serves as the much needed pathognomonic symptom that serves to identify AOS. There is no such pathognomonic symptom in DAS, thereby making diagnosis so much more complex. AOS may be the result of stroke, tumor, or severe damage or trauma to the brain, particularly the left hemisphere which plays a significant role in speech production. AOS also has a genetic basis. DAS has also been defined as a neurogenic disorder and this implies that brain damage is somehow involved despite the continuing lack of evidence. Studies along this line in children with suspected DAS has been further complicated as there may be delayed effect or the elapse of a considerable amount of time before brain damage is manifested overtly. Moreover there is evidence of a genetic basis for DAS. In the words of Caruso and Strand (1991), “Symptoms of acquired and developmental apraxia of speech overlap quite a bit. The most salient features involve articulatory and prosodic disturbances” (p.16). In both DAS and AOS, there are a large number of consonant errors as opposed to vowel errors, which are characterized by omissions and substitutions, errors involve affricates and fricatives, frequency of errors increase as the utterances become longer and increasingly complex, automated or standard responses are less error – prone than spontaneous speech production (Hegde, 2001). These symptoms are not unique to either DAS or AOS and may be evidenced in other speech disorders. Some theorists attribute the causes of AOS to linguistic factors. Shriberg et al., (1997a) have cited “Buckingham’s (1983) perspective on adult AOS as an ‘apraxia of language’[which] places the loci of adult AOS at the level of selection – retrieval of phonemes” (p. 279). This implies that the root cause of AOS appears prior to actual articulation, thereby absolving motor causes. However studies have failed to support this viewpoint. Therefore theorists turned their attention to motor factors which seemed much more plausible. Studies on the deficits of motor programming in DAS have been contradictory and inconclusive as mentioned above. This approach has a much stronger base in AOS, probably as a direct consequence of the research literature supporting its underlying neuropathology. According to Shriberg et al., (1997a) “there is more consensus in the adult AOS literature than in the DAS literature that the type and variability of errors observed in apraxia implicate a programming deficit in motor – speech processing, rather than a planning deficit” (279). Conclusion In DAS as well as AOS the available research literature is inadequate and this has far – reaching implications with regard to clinical aspects as well as treatment procedures. The very existence of DAS has been called into question. A clear definition and a list of diagnostic symptoms are not available for AOS and DAS and furthermore there is a scarcity of knowledge regarding the causes and behavioral manifestations of the disorder. This gives considerable cause for alarm as continuing ignorance on the subject may affect the diagnosis and lower the chances of a favorable prognosis. A proper theoretical framework for both disorders does not exist as ambiguity is the characteristic of the available theories. The use of either of these disorders as a blanket term for speech disorders of unknown origin and confusing symptoms further perpetuates ignorance and confounds treatment procedures. Thus intensive research on DAS and AOS is imperative. References Bahr, R.H., Velleman, S.L., & Ziegler, M.A. (1999). Meeting the challenge of suspected developmental apraxia of speech through inclusion. Topics in Language Disorders, 19(3), 19 – 35. Bishop, D., & Rosenbloom, L. (1987). Classification of childhood language disorders. In W. Yule & M. Rutter (Eds.), Language development and disorders(pp.16 – 41). London: Cambridge University Press. Caruso, A.J., & Strand, E. A. (1999). Motor speech disorders in children: Definitions, Background, and a theoretical framework. In A.J. Caruso & E.A. Strand (Eds.), Clinical management of motor speech disorders in children(pp. 1 – 28). New York: Thieme. Davis, B.L. (2003). Developmental apraxia of speech. In R.D. Kent (Ed), The MIT encyclopedia of communication disorders(pp. 121 – 123). Massachusetts: Massachusetts Institute of Technology Press. Forrest, K., & Marrisette, M.L. (1999). Feature analysis of segmental errors in children with phonological disorders. Journal of Speech. Language, and Hearing Research, 42(1), 187 – 194. Hegde, M.N. (2001). Hegde’s pocketguide to assessment in speech – language pathology. New York: Thomas Delmar Learning. Maassen, B. (2002). Issues contrasting adult acquired versus developmental apraxia of speech. Seminars in Speech and Language, 23(6), 257 – 265. Munson, B., Bjorum, E.M., & Windsor, J. (2003). Acoustic and perceptual correlates of stress in nonwords produced by children with suspected developmental apraxia of speech and children with phonological disorders. Journal of Speech, Language, and Hearing Research, 46(1), 189 – 202. Nijland, L., & Maassen, B. (2005). Syllable planning and motor programming deficits in developmental apraxia of speech. In R.J. Haitsuiker, R. Bastiaanse, A. Postma, & F. Mlijnen (Eds.), Phonological encoding and monitoring in normal and pathological speech (pp. 137 – 154). New York: Psychology Press. Nijland, L., Maassen, B., & van der Meulen, S. (2003). Evidence of motor programming deficits in children diagnosed with DAS. Journal of Speech, Language and Hearing Research, 46(2), 437 – 450. Shriberg, L.D., Aram, D.M., & Kwiatkowski, J. (1997). Developmental apraxia of speech: I descriptive and theoretical perspectives. Journal of Speech, Language and Hearing Research, 40(2), 273 – 285. Shriberg, L.D., Aram, D.M., & Kwiatkowski, J. (1997). Developmental apraxia of speech: II toward a diagnostic marker. Journal of Speech, Language and Hearing Research, 40(2), 286 – 312. Shriberg, L.D., Aram, D.M., & Kwiatkowski, J. (1997). Developmental apraxia of speech: III a subtype marked by inappropriate stress. 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