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. 2017 Apr 14;60(4):S1118–S1134. doi: 10.1044/2016_JSLHR-S-15-0297

Table 1.

Demographic and speech information for a total of 296 of 320 study participants with usable speech samples and determinate Pause Marker (PM) scores.

Group Cohort Title Number of participants
Age (years)
% Male/% female PCC (%)
Samples usable for PM scores Indeterminate PM scores M SD Range M SD Range
Suspected CAS CASI CASI 41 1 9.0 4.2 4–23 68.3/31.7 76.0 13.3 36.8–98.4
CASN a CASN 19 1 10.9 5.2 4–25 47.4/52.6 75.8 12.3 44.9–92.2
Total 60 2 9.7 4.6 4–25 61.7/38.3 76.0 12.9 36.8–98.4
AAS AOS AOS 15 1 62.3 11.6 45–82 73.3/26.7 91.6 7.3 68.9–99.4
PPAOS PPAOS 16 1 71.0 9.0 53–84 56.3/43.7 93.0 6.2 74.0–97.9
Total 31 2 66.8 11.1 45–84 64.5/35.5 92.3 6.6 68.9–99.4
SD Clinical SD1 82 6 4.4 1.3 3–9 74.4/25.6 73.4 12.6 17.5–99.1
Research SD2 22 1 5.5 0.6 5–7 77.3/22.7 82.0 6.9 66.4–91.3
Research SD3 72 12 4.0 0.7 3–5 73.6/26.4 70.0 9.6 36.2–87.2
Research SD4 29 1 4.5 0.9 3–7 48.3/51.7 68.8 11.4 42.1–82.8
Total 205 20 4.4 1.1 3–9 70.7/29.3 72.5 11.5 17.5–99.1
Total all samples 296 24

Note. Speakers comprise two cohorts of participants who were suspected to have childhood apraxia of speech (CAS)—idiopathic CAS (CASI) and neurogenetic CAS (CASN); two cohorts with adult-onset apraxia of speech (AAS): apraxia of speech (AOS) and primary progressive apraxia of speech (PPAOS); and four cohort samples of participants with speech delay (SD).

PCC = percentage of consonants correct.

a

Includes participants with copy-number variants (n = 9) identified in related research and participants with neurodevelopmental disorders associated with disruptions in FOXP2 (n = 2), 4q;16q translocations (n = 3), 16p11.2 microdeletion syndrome (n = 2), terminal deletion of chromosome 22 (n = 1), Joubert syndrome (n = 1), and Prader–Willi syndrome (n = 1).