Abstract

Apraxia of speech (AOS) and childhood apraxia of speech (CAS) are acquired and congenital forms of a neuromotor disorder characterized by deficits in the planning and execution of sequential speech movements in the absence of neuromuscular pathology (McNeil, Robin, & Schmidt, 2009). The childhood and adult forms of the disorder are not directly comparable because of differences in onset and etiology. However, they have been linked because of their speech deficit similarities (Wambaugh, Duffy, McNeil, Robin, & Rogers, 2006; American Speech-Language-Hearing Association, 2007; Shuster & Wambaugh, 2008), and a presumed similarity in impaired neural mechanisms (Jacks & Robin, 2010).