CAS can be congenital, or it can be acquired during speech development. Both congenital and acquired onsets can be idiopathic or can occur in the context of complex neurodevelopmental disorders or in association with a neurological event (Shriberg, 2010). The neurologic deficits underlying CAS are different from those that underlie dysarthria.
CAS, as defined in ASHA, 2007a, can occur
- in association with known neurological etiologies (e.g., intrauterine or early childhood stroke, infection, trauma, brain cancer/tumor resection; e.g., Brown et al., 2000);
- 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);
- as an idiopathic neurogenic speech sound disorder (i.e., children with no observable neurologic abnormalities or neurobehavioral disorders or conditions).
A number of researchers have investigated possible genetic bases for CAS. Of particular interest are findings from studies of the KE family, many of whose members have apraxia of speech. These 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 (e.g., Lai et al., 2000; Lai, Fisher, Hurst, Vargha-Khadem, & Monaco, 2001; Liégeois, Baldeweg, Connelly, Gadian, & Vargha-Khadem, 2003).