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Recent modifications of the lexical model of oral reading make the prediction that under conditions where sublexical reading processes alone cannot achieve the target pronunciation (i.e., when words have exceptional spellings or when sublexical processes are impaired), patients with severe semantic impairment should have more difficulty reading aloud semantically impaired words than semantically retained words. In a battery of lexical-semantic and reading tasks, two neurologically normal control subjects and two subjects with probable Alzheimer's disease (AD) and only moderate semantic impairment read aloud all words accurately. One AD subject with severe semantic impairment was impaired in word reading but demonstrated no difference in reading words with regular and exceptional spellings. Another AD subject with severe semantic impairment read aloud without error virtually all regular and exception words. Neither severely impaired AD subject demonstrated any relationship between oral reading accuracy and semantic knowledge of exception words. These findings support a model of word reading incorporating lexical, nonsemantic processes by which lexical orthographic input representations directly activate lexical phonological output representations without the necessity of semantic mediation. (JINS, 1996, 2, 340–349.)
Humans learn skilled acts in order to effectively interact with their environment. A loss of the ability to perform skilled acts is termed apraxia. Apraxia has been thought to be of theoretical interest, but the ecological implications of apraxia are controversial and have not been fully studied. We examined ten patients with unilateral left hemisphere cerebral infarctions (eight of whom were apraxic) and compared their mealtime eating behavior to a group of neurologically normal, age-matched controls. The stroke patients were less efficient in completing the meal. They made more action errors and were less organized in the sequencing of mealtime activities. Because the patients made more errors while using tools than when performing nontool actions, their deficit could not be accounted for by an elemental motor deficit. A positive relationship was found between mealtime action errors and the severity of apraxia. These findings suggest that limb apraxia may adversely influence activities of daily living. (JINS, 1995, I, 62–66.)
Links between verbs and gesture knowledge suggest that verb retrieval
may be particularly amenable to gesture+verbal training (GVT) in aphasia
compared to noun retrieval. This study examines effects of GVT for noun
and verb retrieval in nine individuals with aphasia subsequent to left
hemisphere stroke. Participants presented an array of noun and verb
retrieval deficits, including impairments of semantic and/or
phonologic processing. In a single-participant experimental design, we
investigated effects of GVT for noun and verb retrieval in two
counterbalanced treatment phases. Effects were evaluated in spoken naming
and gesture production to pictured objects and actions. Spoken naming
improvements associated with large effect sizes were noted for trained
nouns (5/9) and verbs (5/9); no improvements were evident for
untrained words. Gesture production improved for trained nouns (8/9)
and verbs (6/9), and for untrained nouns (2/9) and verbs
(2/9). No significant differences were evident between nouns and verbs
in spoken naming or gesture production. Improvements were evident across
individuals with varied sources of word retrieval impairments. GVT has the
potential to improve communication by increasing spoken word retrieval of
trained nouns and verbs and by promoting use of gesture as a means to
communicate when word retrieval fails. (JINS, 2006, 12,
Past research has shown that lesions in the left cerebral hemisphere
often result in aphasia, while lesions in the right hemisphere frequently
impair the production of emotional prosody and facial expression. At least
3 processing deficits might account for these affective symptoms: (1)
failure to understand the conditions that evoke emotional response; (2)
inability to experience emotions; (3) disruption in the capacity to encode
non-verbal signals. To better understand these disorders and their
underlying mechanisms, we investigated spontaneous affective communication
in right hemisphere damaged (RHD) stroke patients with aprosody and left
hemisphere damaged (LHD) stroke patients with aphasia. Nine aprosodic RHD
patients and 14 aphasic LHD patients participated in a videotaped
interview within a larger treatment protocol. Two naïve raters viewed
segments of videotape and rated facial expressivity. Verbal affect
production was tabulated using specialized software. Results indicated
that RHD patients smiled and laughed significantly less than LHD patients.
In contrast, RHD patients produced a greater percentage of emotion words
relative to total words than did LHD patients. These findings suggest that
impairments in emotional prosodic production and facial expressivity
associated with RHD are not induced by affective–conceptual deficits
or an inability to experience emotions. Rather, they likely represent
channel-specific nonverbal encoding abnormalities. (JINS, 2005,
Patients with probable Alzheimer's disease
(AD) often have difficulties associated with semantic knowledge.
Therefore, conceptual apraxia, a defect of action semantics
and mechanical knowledge, may be an early sign of this
disease. The Florida Action Recall Test (FLART), developed
to assess conceptual apraxia, consists of 45 line drawings
of objects or scenes. The subject must imagine the proper
tool to apply to each pictured object or scene and then
pantomime its use. Twelve participants with Alzheimer's
disease (NINCDS–ADRDA criteria) and 21 age- and education-matched
controls were tested. Nine Alzheimer's disease participants
scored below a 2-standarddeviation cutoff on conceptual
accuracy, and the three who scored above the cutoff were
beyond a 2-standard-deviation cutoff on completion time.
The FLART appears to be a sensitive measure of conceptual
apraxia in the early stages of Alzheimer's disease.
(JINS, 2000, 6, 265–270.)
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