“…By contrast, apraxia of speech (AOS) is acquired later in life following damage to neural structures “responsible for planning and programming motor movements for speech“ (ASHA, 2007), resulting in decreased speech rate and phoneme distortions, among other symptoms (ASHA, 2007). Regarding WM processes, patients with acquired apraxia or dyspraxia of speech have been observed to display, among others: (i) a reduced WM span for words and digits (Ortiz et al, 2010; Rochon et al, 1990; Waters et al., 1991, 1992); (ii) a lack of or reduced word-length and phonological similarity effects (Rochon et al, 1990; Waters et al., 1991; Waters et al, 1992); (iii) chance performance in recognition when asked to indicate whether two probes had been presented previously in the same order (Waters et al, 1991); (iv) a direct relationship between lowered articulation rate and lowered WM span (Waters et al, 1992); and (v) a direct relationship between lowered articulation rate and lowered phonological similarity and word-length effects (lower articulation rate was related to smaller effects; Waters et al, 1992). The pattern of WM deficits described here in patients with apraxia (reduced span and no word-length or phonological similarity effects) can also be observed in normal controls under the condition of articulatory suppression, i.e., when articulatory rehearsal is diminished or unavailable (Baddeley, 1992, 2012; Baddeley et al, 1975).…”