CAS can be congenital, or it can be acquired during speech development. Both congenital and acquired CAS can occur
- as an idiopathic neurogenic speech sound disorder (i.e., in children with no observable neurological abnormalities or neurobehavioral disorders or conditions);
- as primary or secondary signs within complex neurobehavioral disorders (e.g., autism, epilepsy, and syndromes, such as fragile X, Rett syndrome, and Prader–Willi syndrome; Bashina, Simashkova, Grachev, & Gorbachevskaya, 2002; Boyar et al., 2001; Scheffer et al., 1995; Spinelli et al., 1995); or
- in association with known neurological events (e.g., intrauterine or early childhood stroke, infection, trauma, brain cancer/tumor resection; see, e.g., Brown et al., 2000).
The neurological deficits underlying CAS are different from those that underlie dysarthria.
A number of researchers have investigated possible genetic bases for CAS. Of particular interest are findings from studies of a four-generation London family—the KE family—many of whom have apraxia of speech. Findings suggest that deficits in the FOXP2 gene may negatively affect the development of neural networks involved in the learning and/or planning and execution of speech motor sequences (Lai et al., 2000; Lai, Fisher, Hurst, Vargha-Khadem, & Monaco, 2001; Liégeois, Baldeweg, Connelly, Gadian, & Vargha-Khadem, 2003; Marcus & Fisher, 2003; Shriberg et al., 2006; Tomblin et al., 2009; Zeesman et al., 2006).
Recent research continues to find a link between the FOXP2 gene and apraxia of speech, although it is likely that more than one gene is responsible (Adegbola et al., 2015; Laffin et al., 2012; Reuter et al., 2017).