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What defines developmental apraxia of speech How and why does it differ from acquired apraxia of speech - Essay Example

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Very simply explained, DOS is an inability to have verbal communication clarity or speech clarity that is known to result from impaired coordination of the muscles of the articulators(face, tongue, lips, jaw) for the production of speech sounds, syllables or words…
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Extract of sample "What defines developmental apraxia of speech How and why does it differ from acquired apraxia of speech"

What defines developmental apraxia of speech How and why does it differ from acquired apraxia of speech While this is the now the most commonly accepted hypothesis for apraxia overall there is still much debate over differences between developmental and acquired apraxia of speech. There is also much speculation about which of the several theories defining apraxia are the most appropriate. The characterisation of these differences would indeed require a definition and clear understanding of the mechanisms and symptomolgy underlying both the problems. Acquired and developmental apraxia of speech (AOS and DAS) have been defined as disorders which result from dysfunctional shift from the phonological code to motor commands (Maasen2002). However, there is much difference in the natural course of these disorders which is attributed to the elementary difference in the developmental stage at which the apraxia expresses itself initially. We will address both the problems separately in order to acquire a complete picture of these disorders Developmental apraxia of speech (DOS) It is estimated that approximately 60% of children on the ''autism spectrum'' have motor speech dysfunctions; about 13% report primarily symptoms of apraxia; 10% primarily dysarthria while the rest has mixed reports (Marili, Andrianopoulos, Velleman & Foreman,2004). The incidence of primary apraxia in children is perhaps statistically lower. However as these epidemiological studies indicate DOS is considerably prevalent in the society. Very simply explained, DOS is an inability to have verbal communication clarity or speech clarity that is known to result from impaired coordination of the muscles of the articulators(face, tongue, lips, jaw) for the production of speech sounds, syllables or words. It is hypothesised that this disability is caused by neurological malfunctions of certain regions of the brain and not of the muscles themselves. It is primarily associated with children in preadolescent stages of life. Different researchers have identified different means of identifying the disorder in terms of the processes involved. Maasen hypothesis is indicated in the following idea. "a reduced capacity to form systemic mappings [between articulator movements and their auditory consequences might underlie the oral motor and early speech learning difficulties in DOS and put the child at a disadvantage for the acquisition of the motor aspects of phonology, that is, the phoneme-specific mappings" (Maassen 2002). However as Shrenberg has pointed out, this is not the only possibility or by any means adequate for diagnosis. There are several inconsistencies across children furthermore the symptoms are known to change over time (Lewis et al. 2004; Shriberg et al. 2003). Given the incidence of such discrepancies the question that much of the clinical world and scientific community is struggling with is the diagnosis of the dysfunction. Reliable differential diagnosis The various symptoms related with AOS often overlap or occur simultaneously with deficits produced by other neuromuscular deficits the linguistic errors associated with such conditions. However AOS is a distinctive motor speech disorder that can occur independently. It is hence vital to make adequate diagnosis. However as Neil has correctly identified a lack of clear operational diagnostic criterion (Neil 2001) are one of the major hurdles for clinicians today. On the grounds that primary deficit in DAS is still divisive Shriberg et al (!997) had concluded that exclusion of other symptoms was the only available diagnostic marker. However this is now known to be changing although the progress is slow. Apraxia is often confused with conduction aphasia and much less frequently with dysarthria. However, evidently all these speech disorders are distinctly different in their eteiology. Reliable diagnosis is the key in this respect. Aphasia is manifested as an underlying deficit in the selection of the phonemes for the articulation process and hence for speech resulting in a language deficit. Apraxic speakers, on the other hand, are able to select the correct phonemes are unable to perform the motor execution adequately. AOS also diverges from dysarthria aetiology. While impairment of muscle strength and tone, or coordination is explicitly the cause for the former AOS is not caused by these factors. (Darley et al., 1975). It has been suggested that central nervous system damage (lesions) is the primary cause of apraxia. It has been suggested that there are some characteristics of pure AOS that are unique to the disorder. These are sound distortions, prolonged segment durations (e.g., prolonged vowels or consonants) and prolonged intersegment durations (e.g., abnormal pauses (McNeil et al., 2004). This is increasingly being used in the clinic to make differential diagnosis. Acquired Apraxia of speech (aAOS) While apraxia in children (DAS) is distinct from other speech disorders it is suggested to be relatively more closely associated with Apraxia of speech in adults (Shriberg 2003). How does this impairment happen in adults who have already mastered the articulation and phonological encoding processes unlike infants who are still in the learning process shall be discussed further on. It has been suggested that aAOS is a lesion specific in its incidence unlike DAS which is not necessarily based on the occurrence of lesions in the brain . This could perhaps be an explanatory hypothesis. Speech process it is suggested is comprised of phonological planning, retrieval of the word and encoding followed by motor articulation of the plan in adults (Maasen 2002).In children the process is much simplified. Furthermore the articulomotor senses and the phonological coding regions are distinct and different in adults as opposed to in children where an interaction of sorts between the two is observed. This is hypothesised to form the basis of the differences in adult and pre adult stage speech patterns. This also forms, as a consequence, the differential pattern of apraxia in children and adults. A disorder of motor planning and motor programming in the cognitive processing, results, in an impairment of the phonological encoding that has been previously described. It is possible that that in the biological cascade of events it is the impairment at this level that causes the problem. The search for a marker for diagnostic purposes is still ongoing for both DOS and acquired AOS. However since the incidence of the dysfunction independent of other disorders is not as common to find such a marker poses a serious challenge. Treatment (motor or cognitive) It is observed that practice and directed training facilitate progress in attenuation of therapy for childhood apraxia of speech (DOS). It is suggested that since motor learning deficits such as DOS are controlled by areas relating to cognition in the central nervous system it is possible to acquire or learn. Furthermore, incidence of apraxia in adults is often coupled with the presence of additional cognitive and motor impairments as has been shown in studies by Heugten and his colleagues. This while providing for an effective combat strategy cats some doubts on the validity of the theories which have been known to underly apraxia. If indeed neuropathological lesions deficits alone are the basis of the aetiology (Duffy, 1995), then it would have been difficult for training to have beneficial effect. It can hence be derived that both adult and developmental forms of the dysfunction are strongly affected by the cognitive and motor derailments of neuronal circuits that can be conditioned (DOS) or reconditioned (AOS) in order to build adequate treatment strategies. Sound-based manoeuvring via 'alliteration, rhyming, and deletion' of specific word and sounds are suggested to go a long way to improve phonological awareness and the aptitude to encode sounds in children in particular. Conclusion In terms of the way to go, it would perhaps be efficacious to view and define Apraxia of speech as a collection of symptoms as observed in several other neurological disorders that together have been recognized as a singular motor speech disorder. For instance, some of the language/speech deficits allied to AOS are apparently motor derived (e.g., groping) and others more language-like (e.g., transpositions). The variety of AOS-like motor speech deficits have been allied with a rather extended range of lesion sites and neuropathological deficits, including the insula, frontal, and temporoparietal regions, as well as subcortical white matter areas (Square & Martin, 1994). In effect it appears that several varied brain regions have a role in distinct ways to motor speech production and hence to the aberrance that results in apraxia both developmental and acquired. While science has yet to provide adequate diagnostic markers for the defect, the present literature on the subject provides some measures to combat the threats posed by this rather serious health hazard that a significant percentage of the populations is struggling with for the past several decades. Sources Darley, FL, Aronson, AE, and Brown, JR Motor Speech Disorders-Audio Tapes W.B. Saunders: Philadelphia, (1975). Duffy,J (1995) Motor speech disorders, Mosby, St. Louis Heugten CM et al (2000). Rehabilitation of stroke patients with apraxia: the role of additional cognitive and motor impairments. Disabil Rehabil.;22(12):547-54 Lewis, B.A., Freebairn, L.A., Hansen, A.J., Iyengar, S.K. & Taylor, H.G. (2004). Schoolage follow-up of children with Childhood Apraxia of Speech. Language, Speech, and Hearing Services in Schools 35(2): 122 -140. Maassen, B. (2002). Issues contrasting adult acquired versus developmental apraxia of speech. Seminars in Speech and Language, 23(4), 257-266. Marili, K. E., Andrianopoulos, M. V., Velleman, S. L., & Foreman, C. G. (2004, November). Incidence of motor speech impairment in autism and Asperger's disorders.Paper presented at the American Speech-Hearing-Language Association Convention,Philadelphia. McNeil MR. The assiduous challenge of defining and explaining apraxia of speech. In: Maassen B, Hulstijn W, Kent RD, Peters HFM, van Lieshout PHHM, eds. Speech Motor Control in Normal and Disordered Speech. Proceedings of the 4th International Speech Motor Conference; June 13-16, 2001; Nijmegen, The Netherlands; Nijmegen: Uitgeverij Vantilt; 2001:337-342 McNeil, MR, Pratt, SR, and Fossett, TRD The differential diagnosis of apraxia of speech. In Speech motor control in normal and disordered speech Maassen, B, Ed.; Oxford University Press: New York, (2004): 389-412. Shriberg LD, Aram DM, Kwiatkowski J. Developmental apraxia of speech. I. Descriptive and theoretical perspectives. J Speech Lang Hear Res 1997; 40:273-285 Shriberg, L. D., Campbell, T. F., Karlsson, H. B., Brown, R. L., McSweeny, J. L., & Nadler, C. J. (2003). A diagnostic marker for childhood apraxia of speech: The lexical stress ratio. Clinical Linguistics and Phonetics, 17(7), 549-574. Shriberg, L. D., Green, J. R., Campbell, T. F., McSweeny, J. L., & Scheer, A. R. (2003). A diagnostic marker for childhood apraxia of speech: The coefficient of variation ratio. Clinical Linguistics and Phonetics, 17(7), 575-595. Square PA and Martin,RE (1994) The nature and treatment of neuromotor speech disorders in aphasia. In: R. Chapey, Editor, Language intervention strategies in adult aphasia, Williams and Wilkins, Baltimore pp. 467-499. Strand, E. A. (1995). Darley's contributions to the understanding and diagnosis of developmental apraxia of speech. Aphasiology, 15(2), 291-304. Strand, Edythe A. (1995). Treatment of motor speech disorders in children. Seminars inSpeech and Language, 16(2), 126- 139. Read More
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