Table 9.
Charting of acquired apraxia of speech (AOS) studies in neuroimaging category.
| Study | Participants |
Method/task | Dependent measures | Main results | Sensitivity/specificity? | |
|---|---|---|---|---|---|---|
| Group | n | |||||
| Josephs et al. (2006) | prAOS | 7 | MRI-structural, SPECT, pathology, behavioral assessment | GM, WM atrophy | - AOS was primarily associated with atrophy in the premotor and supplementary motor cortices - All AOS cases had a pathological diagnosis characterized by underlying tau biochemistry |
N |
| prAPH + AOS | 3 | |||||
| prAPH | 7 | |||||
| Josephs et al. (2012) | prAOS | 12 | MRI-structural, DTI, PiB-PET, FDG-PET, behavioral assessment | GM, WM atrophy; fractional anisotropy; mean diffusivity; voxel-wise metabolism | - For prAOS group compared to HC, GM atrophy was focused in superior lateral premotor cortex and supplementary motor area; WM loss was also focused in these regions + inferior premotor cortex and body of corpus callosum - prAOS group showed reduced fractional anisotropy and increased mean diffusivity of the superior longitudinal fasciculus - prAOS groups showed hypometabolism of superior lateral premotor cortex and supplementary motor area |
N |
| HC | 24 | |||||
| Josephs et al. (2013) | prAOS | 18 | MRI-structural, DTI, PiB-PET, FDG-PET, behavioral assessment | GM, WM atrophy; fractional anisotropy; mean diffusivity; voxel-wise metabolism | - Both proAOS and prAOS + APH groups showed atrophy and hypometabolism in premotor cortex and midbrain, whereas prAPH groups showed imaging abnormalities in premotor, prefrontal, temporal, parietal lobes + caudate, insula | N |
| prAOS + APH | 10 | |||||
| prAPH | 9 | |||||
| HC | 30 | |||||
| Trupe et al. (2013) | strAOS + APH | 17 | MRI-structural, behavioral assessment | Voxel intensity vs. ABA-2 scores (voxel-based lesion–symptom mapping) | - AOS was associated with infarct in Broca's area, anterior temporal cortex, and posterior insula; AOS severity was positively correlated with lesion volume | N |
| strAPH | 17 | |||||
| Whitwell, Duffy, Strand, Machulda, et al. (2013) | prAOS | 16 | MRI-structural, DTI, behavioral assessment | GM, WM atrophy; fractional anisotropy; mean diffusivity | - Both PPAOS and NOS (dx = PSP-S) groups showed GM atrophy in supplementary motor area and WM atrophy in posterior frontal lobes - PPAOS group showed more focal GM atrophy in superior premotor cortex compared to more widespread (extending into prefrontal cortex) atrophy in PSP-S group |
N |
| NOS | 16 | |||||
| HC | 20 | |||||
| Whitwell, Duffy, Strand, Xia, et al. (2013) | prAOS | 17 | MRI-structural, FDG-PET, behavioral assessment | GM atrophy, hypometabolism | - The left superior premotor volume was the only region that correlated with AOS severity (measured using the ASRS) - Neither inferior posterior frontal cortex (i.e., Broca's area) nor insula correlated with AOS severity; Broca's area instead correlated with severity of agrammatism |
N |
| prAOS + APH | 18 | |||||
| prAPH | 1 | |||||
| Caso et al. (2014) | nfvPPA (FTLD-tau) | 9 | MRI-structural, pathology, behavioral assessment | GM, WM atrophy; AOS severity ratings | - AOS was the most common feature at presentation regardless of FTLD subtype - prAOS (FTLD-tau) characterized by atrophy in GM of left posterior frontal regions and left frontal WM - prAOS (FTLD-TDP) characterized by atrophy in left posterior frontal GM only |
N |
| nfvPPA (FTLD-TDP) | 2 | |||||
| Josephs et al. (2014) | prAOS | 13 | MRI-structural, DTI, FDG-PET, behavioral assessment | Rates of whole-brain, ventricle, and midbrain volume atrophy; rates of regions GM atrophy, WM tract degeneration | - prAOS group had elevated rates of whole-brain atrophy, ventricular expansion, and midbrain atrophy - Increased rates of atrophy for prAOS group in prefrontal cortex, motor cortex, basal ganglia, and midbrain |
N |
| HC | 20 | |||||
| Mandelli et al. (2014) | prAOS + APH | 9 | MRI-structural, DTI, behavioral assessment | Tract-specific DTI metrics | - Significant WM changes in the left intrafrontal and frontostriatal pathways were found in nfvPPA, but not in lvPPA or svPPA - Correlations between tract-specific DTI metrics suggested a preferential role of a posterior premotor–SMA pathway in motor speech/AOS |
N |
| prAPH | 16 | |||||
| HC | 21 | |||||
| Basilakos et al. (2015) | strAOS + APH | 18 | MRI-structural, behavioral assessment | Voxel intensity vs. ASRS scores (voxel-based lesion–symptom mapping) | - Patterns of brain damage were at least partially dissociable for strAOS + APH vs. strAPH groups; AOS was most strongly associated with damage to cortical motor regions and somatosensory areas | N |
| strAPH | 16 | |||||
| Botha et al. (2015) | prAOS | 40 | MRI-structural, DTI | GM atrophy, fractional anisotropy, mean diffusivity | - Compared to controls, PPAOS group shows GM atrophy in bilateral premotor and SMA regions, middle cingulate gyri, Broca's area, insular gray matter. DTI abnormalities were observed in same regions and also implicated left uncinate fasciculus and bilateral superior longitudinal fasciculi - Direct comparison of PPAOS and nfvPPA groups revealed greater GM atrophy for nfvPPA group in left temporal, hippocampus and fusiform gyrus |
N |
| prAOS + APH | 12 | |||||
| prAPH | 52 | |||||
| NOS | 26 | |||||
| New et al. (2015) | strAOS + APH | 15 | fMRI (resting state), behavioral assessment | Mean gray, white matter signal intensity | - strAOS + APH group showed reduced connectivity between bilateral premotor regions; reduction of connectivity correlated with AOS severity | N |
| strAPH | 17 | |||||
| HC | 18 | |||||
| Itabashi et al. (2016) | strAOS | 7 | MRI-structural, behavioral assessment | Voxel intensity vs. diagnosis (voxel-based lesion–symptom mapping) | - Brain regions associated with AOS were centered on the left precentral gyrus | N |
| strAOS + APH | 15 | |||||
| DC | 114 | |||||
| Cerami et al. (2017) | prAOS + APH | 19 | FDG-PET, behavioral assessment | Voxel-wise metabolism | - Hypometabolism patterns differed across subtypes; among nfvPPA patients, parietal, subcortical and brainstem hypometabolism predict progression to corticobasal syndrome or progressive supranuclear palsy | N |
| prAPH | 28 | |||||
| prDYS | 3 | |||||
| NOS | 5 | |||||
| Botha et al. (2018) | prAOS | 22 | fMRI (resting state), MRI-structural, behavioral assessment | Gray, white matter signal intensity in intrinsic connectivity networks (ICNs); connectivity vs. apraxia severity (ASRS scores) | - prAOS group showed reduced connectivity in speech and language, face, salience, and left working memory ICNs - Reduced connectivity for prAOS group between right SMA and rest of speech and language ICN, which correlated with AOS severity |
N |
| HC | 44 | |||||
| Utianski, Whitwell, Schwarz, Duffy, et al. (2018) | prAOS + APH | 5 | MRI-structural, tau-PET | Tau uptake, measured using ratio of cortical to cerebellar signal (SUVr) in ROIs | - Compared to HC group, prAPH groups showed uptake of tau in left frontal and parietal regions of interest, whereas prAOS + APH group showed uptake in bilateral SMA, frontal lobes, precuneus, and precentral gyrus - prAOS + APH showed greater tau uptake in left precentral gyrus compared to prAPH group |
N |
| prAPH | 4 | |||||
| HC | 27 | |||||
| Utianski, Whitwell, Schwarz, Senjem, et al. (2018) | prAOS | 7 | MRI-structural, tau-PET, PiB-PET | Tau uptake (SUVr), ROI level and voxel level | - Compared to HC group, both prAOS + APH groups showed increased tau uptake in SMA, precentral gyrus, and Broca's area - prAOS group showed pattern of increased tau uptake only in superior (incl. SMA) and premotor cortices, and not in Broca's area |
N |
| prAOS + APH | 7 | |||||
| HC | 42 | |||||
| Utianski et al. (2019) | prAOS | 3 | EEG, MRI-structural | Posterior dominant rhythm; clinical EEG read | - Patients with aphasia (prAPH and prAOS + APH groups) demonstrated theta slowing whereas the AOS-only group (prAOS) did not, and instead showed normal EEG patterns | N |
| prAOS + APH | 2 | |||||
| prAPH | 3 | |||||
Note. pr = progressive etiology; AOS = a group with apraxia and no comorbid language deficits (dysarthria status not accounted for); MRI-structural = structural magnetic resonance imaging; SPECT = single-photon emission computed tomography; GM = gray matter; WM = white matter; N = no; APH = a group with aphasia-only deficits (no AOS); DTI = diffusion tensor imaging; PiB = Pittsburgh compound B; PET = positron emission tomography; HC = healthy control; FDG = fluorodeoxyglucose; AOS + APH = AOS group with comorbid language impairment; str = poststroke or other acute acquired etiology; ABA-2 = Apraxia Battery for Adults–Second Edition; PPAOS = primary progressive apraxia of speech; NOS = diagnosis not otherwise specified, e.g., semantic dementia, unclassified primary progressive aphasia cases, behavioral variant frontotemporal dementia, progressive supranuclear palsy; dx = diagnosis; PSP-S = progressive supranuclear palsy syndrome; ASRS = Apraxia of Speech Rating Scale; nfvPPA = nonfluent variant primary progressive aphasia; FTLD-tau = frontotemporal lobar degeneration with tau pathology; FTLD-TDP = frontotemporal lobar degeneration with TDP-43 inclusions; lvPPA = logopenic variant primary progressive aphasia; svPPA = semantic variant primary progressive aphasia; SMA = supplementary motor area; fMRI = functional magnetic resonance imaging; DC = other disease control (e.g., individuals who have had a stroke but with no AOS or aphasia); DYS = dysarthria-only group (no AOS, no aphasia); SUVr = standardized uptake value ratio; ROIs = regions of interest; EEG = electroencephalography.