118 research outputs found

    Repeated attempts, phonetic errors, and syllabifications in a case study:Evidence of impaired transfer from phonology to articulatory planning

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    Background: In aphasia, impairments affecting stages after lexical access have been subdivided into three types: 1. impairments specifying a sequence of phonemes after lexical access (the reproduction variety of conduction aphasia, CA); 2. impairments holding on to these representations during articulatory planning (the short-term memory (STM) variety of CA); and 3. Impairments specifying integrated articulatory/motor plans for clusters of phonemes (apraxia of speech, AoS). Models of speech production, however, suggest more articulated possibilities (i.e., different subtypes of articulatory impairments). Aims: We investigated the impairment in a person with aphasia whose preliminary assessment revealed mixed speech characteristics, combining features typically used to identify CA – phonological errors across tasks and repeated attempts at the target – with features typically used to identify AoS – phonetic errors and word dysfluencies (phoneme elongations and syllabifications). Our preliminary hypothesis was that there was a difficulty transferring information from an (intact) phonological output buffer to articulatory planning. Slow/noisy transfer would predict dysfluencies, errors selecting motor programs, but also repeated attempts (RA) at revising the output in the face of intact feedback and intact original representations. This hypothesis also predicts effects of position and phonological complexity. Method and Procedure: We tested CS’s word and nonword repetition, word reading, and picture naming. We quantified lexical and non-lexical errors, repeated attempts, phonetic errors, and syllabifications. We assessed effects of word frequency, word length, phoneme position, and syllabic and phonological complexity. Results: CS made similar errors across tasks, consistent with a post-lexical impairment. His RAs most often built up a correct target from fragments and/or previously incorrect attempts, similar to a conduite d’approche. He also produced more errors in later positions, and more repeated attempts on longer words. However, inconsistent with decay from an output buffer, phonological errors did not increase with word length. Finally, frequency mattered, consistent with easier/faster access to simpler/more practiced motor plans. Conclusions: CS’s speech characteristics and anatomical lesion are consistent with transfer limitations between phonology and articulatory planning. However, CS has more difficulties in computing articulatory plans than in selecting and retaining phonological representations, as commonly attributed to CA. CS’s case suggests that different varieties of phonological and articulatory disorders need to be distinguished, beyond a strict dichotomy AoS/CA (e.g., involving transfer limitations and difficulties in computing, selecting,, and/or initiating articulatory plans)

    An EMA analysis of the effect of increasing word length on consonant production in apraxia of speech: A case study

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    The effect of increasing word length on the articulatory dynamics (i.e. duration, distance, maximum acceleration, maximum deceleration, and maximum velocity) of consonant production in acquired apraxia of speech was investigated using electromagnetic articulography (EMA). Tongue-tip and tongue-back movement of one apraxic patient was recorded using the AG-200 EMA system during word-initial consonant productions in one, two, and three syllable words. Significantly deviant articulatory parameters were recorded for each of the target consonants during one, two, and three syllables words. Word length effects were most evident during the release phase of target consonant productions. The results are discussed with respect to theories of speech motor control as they relate to AOS

    Apraxia in progressive nonfluent aphasia

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    The clinical and neuroanatomical correlates of specific apraxias in neurodegenerative disease are not well understood. Here we addressed this issue in progressive nonfluent aphasia (PNFA), a canonical subtype of frontotemporal lobar degeneration that has been consistently associated with apraxia of speech (AOS) and in some cases orofacial apraxia, limb apraxia and/or parkinsonism. Sixteen patients with PNFA according to current consensus criteria were studied. Three patients had a corticobasal syndrome (CBS) and two a progressive supranuclear palsy (PSP) syndrome. Speech, orofacial and limb praxis functions were assessed using the Apraxia Battery for Adults-2 and a voxel-based morphometry (VBM) analysis was conducted on brain MRI scans from the patient cohort in order to identify neuroanatomical correlates. All patients had AOS based on reduced diadochokinetic rate, 69% of cases had an abnormal orofacial apraxia score and 44% of cases (including the three CBS cases and one case with PSP) had an abnormal limb apraxia score. Severity of orofacial apraxia (but not AOS or limb apraxia) correlated with estimated clinical disease duration. The VBM analysis identified distinct neuroanatomical bases for each form of apraxia: the severity of AOS correlated with left posterior inferior frontal lobe atrophy; orofacial apraxia with left middle frontal, premotor and supplementary motor cortical atrophy; and limb apraxia with left inferior parietal lobe atrophy. Our findings show that apraxia of various kinds can be a clinical issue in PNFA and demonstrate that specific apraxias are clinically and anatomically dissociable within this population of patients
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