Honors Theses and Capstones

Date of Award

Spring 2021

Project Type

Senior Honors Thesis

College or School

CHHS

Department

Communication Sciences and Disorders

Program or Major

Communication Sciences and Disorders

Degree Name

Bachelor of Science

First Advisor

Donald Robin

Abstract

The theories and neural bases of Apraxia of Speech (AOS) have long been debated. In 1861, Paul Broca identified two patients with speech/language impairments who became the basis for the theory on aphemia, now known as apraxia. Broca noted of patients with AOS that “there are cases in which the general faculty for language remains unaltered; where the auditory apparatus is intact; where all muscles—including those of speech and articulation—are under voluntary control; and where nevertheless, a cerebral lesion abolishes articulated language” (Broca, 1861/2000). The term “apraxia” was first introduced by Hugo Liepmann in 1908 and was described as “the inability to perform voluntary acts despite preserved muscle strength” (Liepmann, 1908). Darley then coined the term “apraxia of speech” in 1969 (Darley et al., 1969).

The American Speech and Hearing Association (ASHA) defines Apraxia of Speech as a “neurologic speech disorder that reflects an impaired capacity to plan or program sensorimotor commands necessary for directing movements that result in phonetically and prosodically normal speech” (Duffy, 2013). The perceptual characteristics of the disorders are described by ASHA as “(a) phoneme distortions and distorted substitutions or additions (b) reduced overall speech rate (c) syllable segregation with extended intra- and intersegmental durations and (d) equal stress across adjacent syllables” (Acquired Apraxia of Speech, n.d.). These characteristics reflect some of the initial clinical features identified by Darley (1969). These symptoms are relatively similar to the current diagnostic criteria of AOS established by (McNeil et al., 2009) except that symptoms are currently described as increased inter and intra segmentation, sound distortions, abnormal prosody, and does not reflect slower rate of speech. McNeil et al. would argue that it is distortions which are the critical diagnostic feature, rather than substitutions and additions. However, these errors do co-occur as many individuals with AOS or CAS have accompanying phonological impairments.

In 2000, Ballard, Granier, and Robin conducted a critical review of acquired apraxia of speech (AOS) focusing on different theories and supportive research. The review also explored intervention models associated with AOS (Ballard et al., 2000). Since that time, extensive work in AOS has been conducted, existing models of the disorder have been refined, and new models have been proposed. In addition, new information on childhood apraxia of speech (CAS) has emerged and theories related to CAS require critical evaluation. In particular, the relationship between stroke related AOS and CAS is critical to advancing efforts in this area. The purpose of this paper is to update Ballard and colleagues (2000) and expand the information to include CAS. (Ballard et al., 2000) hypothesized that the deficits demonstrated in individuals with apraxia of speech could be due to phonological processing, motor control or both. It is now accepted that AOS is a disorder of motor control. In this paper, the most recent research regarding the theoretical understanding of AOS, as well as neural models will be presented. Treatments for AOS will be reviewed and evaluated for efficacy. This paper covers the history of AOS starting with (Darley, 1975).

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