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1 n published a 'Schema for the Examination of Aphasic and Amnesic Persons'.
2 tion as well as functional imaging in stroke aphasic and neurologically intact participants.
3 endering the patient quadriparetic, globally aphasic, and minimally responsive.
4 ual pathway, nor any synthesis of normal and aphasic behavior.
5                                          One aphasic case displayed higher right-hemisphere tangle de
6 inal tangles was significantly higher in the aphasic cases (P = 0.034).
7 ocampus and/or entorhinal cortex) in several aphasic cases and the severe occipito-parietal involveme
8 ged from neuropsychological studies in other aphasic cohorts, and functional imaging studies in healt
9 euroimaging work with progressive non-fluent aphasics, compared directly to non-aphasic patients with
10                                              Aphasic deficits are usually only interpreted in terms o
11  of ADNC in typical amnestic versus atypical aphasic dementia and of TDP in type A versus type C reve
12 band and an affected brother had progressive aphasic dementia, leukoencephalopathy, and occipital cal
13  clinical profile did not include non-fluent aphasic features.
14                     We found that, while the aphasic groups were impaired relative to normal controls
15                                Five of seven aphasics had more leftward tangle asymmetry in all four
16  structurally disconnected regions relate to aphasic impairment and its recovery.
17 emic differences for control subjects versus aphasics in left primary auditory cortex and bilateral s
18                              The most common aphasic manifestation was of the logopenic type for Alzh
19         The same region was activated in the aphasic patients as they listened to standard (undistort
20 andard test of spoken language in 16 chronic aphasic patients both before and after a rehabilitation
21                                  As a group, aphasic patients demonstrated a selective disruption of
22 compare SD and comprehension-impaired stroke aphasic patients directly on the same battery of semanti
23 to characterize a large group of progressive aphasic patients from a single center (n = 38), first cl
24 entification of Alzheimer pathology in these aphasic patients is puzzling since tangles and related n
25 graphy) and word rate in normal subjects and aphasic patients listening to monosyllabic words at rate
26                             In addition, the aphasic patients made associative semantic errors in pic
27                                     Severely aphasic patients tended to perform worse in both domains
28 ng the ability of 30 left hemisphere-damaged aphasic patients to match environmental sounds and lingu
29                   Preliminary experiments in aphasic patients using transcranial magnetic stimulation
30                                      Chronic aphasic patients were impaired at the task and demonstra
31 ol groups: 12 normal subjects and 7 anterior aphasic patients whose infarcts spared the left POp.
32 on-fluent aphasics, compared directly to non-aphasic patients with frontotemporal dementia, has demon
33                             We studied seven aphasic patients with left anterior perisylvian infarcti
34  the neuropsychology component of the study, aphasic patients with multimodal semantic deficits follo
35              Subgroup analysis revealed that aphasic patients with preserved positive intertemporal c
36                                          The aphasic patients' picture naming performance improved co
37 sfunctional in comprehension-impaired stroke aphasic patients).
38 paring and impairment of those structures in aphasic patients, and the structures that normal adults
39 bust predictor of impaired speech fluency in aphasic patients, even when motor speech, lexical proces
40  Here we demonstrate for the first time that aphasic patients, who have largely recovered language fu
41  types of data from healthy participants and aphasic patients.
42 d a detailed set of procedures for examining aphasic patients.
43 may even be useful for enhancing recovery in aphasic patients.
44  Asymmetric cortical degeneration syndromes (aphasic, perceptual-motor, frontal lobe and bitemporal c
45  separating the principal aspects of chronic aphasic performance and isolating their neural bases.
46  concordance of Alzheimer pathology with the aphasic phenotype.
47 etry of cortical atrophy consistent with the aphasic phenotype.
48                                          The aphasic presentations include both fluent and non-fluent
49 in normal speakers and damage to the LIFG in aphasic speakers was associated with performance on the
50 he results of lesion-deficit correlations in aphasic speakers who performed the same word production
51 amage to those regions results in non-fluent aphasic speech; when they are undamaged, fluent aphasias
52 ed sensitivity to phonemic boundaries in the aphasics' speech network in both hemispheres.
53 een language comprehension performance after aphasic stroke and the functional connectivity of a key
54                Although many more studies of aphasic stroke are required with larger patient numbers
55 left and right ATLs in patients with chronic aphasic stroke has been illustrated.
56 studies investigating language outcome after aphasic stroke have tended to focus only on the role of
57 y in the recovery of speech production after aphasic stroke may relate in part to differences in pati
58          Functional neuro-imaging studies of aphasic stroke offer the potential for a better understa
59 al cortex connectivity in a group of chronic aphasic stroke patients.
60 as posterior regions described in studies on aphasic stroke patients.
61 n the impaired speech production observed in aphasic stroke patients.
62 a marker of receptive language outcome after aphasic stroke, and illustrate that language system orga
63 ntact neural networks promote recovery after aphasic stroke, either spontaneously or in response to i
64 en that this brain region is often spared in aphasic stroke, we propose that it is a sensible target
65 tributing to the potential for recovery from aphasic stroke.
66 ral superior temporal cortex connectivity in aphasic stroke.
67 ence comprehension following left hemisphere aphasic stroke.
68  one factor that may determine recovery from aphasic stroke.
69 nguage assessments are useful for diagnosing aphasic syndromes and for characterizing other disorders
70 e clinical classification of the progressive aphasic syndromes is also debated.
71 tia within the classification of progressive aphasic syndromes, and for contemporary models of semant
72 entations include both fluent and non-fluent aphasic syndromes.
73 s of tangles and plaques were greater in the aphasic than amnestic cases (P < 0.05), especially in ne
74  speech patterns of each primary progressive aphasic variant adequately, and to reveal associations b
75                                   Within the aphasics, we also found behavioural correlates with conn
76 9 prospectively enrolled primary progressive aphasics were selected for this study because of peak at
77 port the performance of two Italian-speaking aphasics who show contrasting, selective difficulties in
78                     Our results suggest that aphasics with impaired speech comprehension have less ve
79  stages and processes involved in normal and aphasic word production.
80 sonance imaging, to 14 chronic patients with aphasic word retrieval deficits.