Sub-classification of apraxia of speech in patients with cerebrovascular and neurodegenerative diseases.

Some studies have hypothesized that primary progressive apraxia of speech (ppAOS) consists of heterogeneous symptoms that can be sub-classified; however, no study has classified stroke-induced AOS (sAOS) and ppAOS according to common criteria. The purpose of this study was to elucidate the symptoms and relevant brain regions associated with sAOS and ppAOS for sub-classification. Participants included 8 patients with sAOS following lesions in the left precentral gyrus and/or underlying white matter, and 3 patients with ppAOS. All patients with sAOS could be classified into three subtypes: type I, with prominent distorted articulation; type II, with prominent prosodic abnormalities or type III, with similarly distorted articulation and prosodic abnormalities. This sub-classification was consistent with the subtypes of ppAOS proposed in previous reports. All patients with ppAOS were classified as type III, and exhibited three characteristics distinguishable from those of sAOS. First, they showed prominent lengthened syllables compared with the segmentation of syllables. Second, they could not always complete the production of multi-syllabic single words in one breath. Finally, they showed dysfunctional lesions in the bilateral supplementary motor area. We conclude that sAOS and ppAOS can be sub-classified and are universal symptoms that are common between the English and Japanese populations.

[Networks involved in motor cognition : Physiology and pathophysiology of apraxia]. / Netzwerke für motorische Kognition : Physiologie und Pathophysiologie der Apraxie.

Apraxia is an umbrella term for different disorders of higher motor abilities that are not explained by elementary sensorimotor deficits (e. g. paresis or ataxia). Characteristic features of apraxia that are easy to recognize in clinical practice are difficulties in pantomimed or actual use of tools as well as in imitation of meaningless gestures. Apraxia is bilateral, explaining the cognitive motor disorders and occurs frequently (but not exclusively) after left hemispheric lesions, as well as in neurodegenerative diseases, such as corticobasal syndrome and Alzheimer's disease. Apraxic deficits can seriously impair activities of daily living, which is why the appropriate diagnosis is of great relevance. At the functional anatomical level, different cognitive motor skills rely on at least partly different brain networks, namely, a ventral processing pathway for semantic components, such as tool-action associations, a ventro-dorsal pathway for sensorimotor representations of learnt motor acts, as well as a dorso-dorsal pathway for on-line motor control and, probably, imitation of meaningless gestures. While these networks partially overlap with language-relevant regions, more clear cut dissociations are found between apraxia deficits and disorders of spatial attention. In addition to behavioral interventions, noninvasive neuromodulation approaches, as well as human-computer interface assistance systems are a growing focus of interest for the treatment of apraxia.

Utility of testing for apraxia and associated features in dementia.

INTRODUCTION: Existing literature suggests that the presence or absence of apraxia and associated parietal deficits may be clinically relevant in differential diagnosis of dementia syndromes. AIM: This study investigated the profile of these features in Alzheimer's disease (AD) and frontotemporal dementia (FTD) spectrum disorders, at first presentation. METHODS: Retrospective case note analysis was undertaken in 111 patients who presented to the Oxford Cognitive Disorders Clinic, Oxford, UK, including 29 amnestic AD, 12 posterior cortical atrophy (PCA), 12 logopenic primary progressive aphasia (lvPPA), 20 behavioural variant FTD (bvFTD), 7 non-fluent variant PPA (nfvPPA), 6 semantic variant PPA (svPPA) and 25 patients with subjective cognitive impairment (SCI). The clinical features of interest were: limb apraxia, apraxia of speech (AOS), and left parietal symptoms of dyslexia, dysgraphia, and dyscalculia. RESULTS: The prevalence of limb apraxia was highest in PCA, amnestic AD, lvPPA and nfvPPA. AOS was only observed in nfvPPA. Associated parietal features were more prevalent in AD spectrum than FTD spectrum disorders. Group comparisons between key differential diagnostic challenges showed that lvPPA and nfvPPA could be significantly differentiated on the presence of left parietal features and AOS, and amnestic AD could be differentiated from bvFTD, svPPA and SCI by limb apraxia. Regression analysis showed that limb apraxia could successfully differentiate between AD and FTLD spectrum disorders with 83% accuracy. DISCUSSION: Disease-specific profiles of limb apraxia and associated deficits can be observed. FTD and AD spectrum disorders can be difficult to differentiate due to overlapping cognitive symptoms, and measures of apraxia, in particular, appear to be a promising discriminator.

Social communication disorder outside autism? A diagnostic classification approach to delineating pragmatic language impairment, high functioning autism and specific language impairment.

BACKGROUND: Developmental disorders of language and communication present considerable diagnostic challenges due to overlapping of symptomatology and uncertain aetiology. We aimed to further elucidate the behavioural and linguistic profile associated with impairments of social communication occurring outside of an autism diagnosis. METHODS: Six to eleven year olds diagnosed with pragmatic language impairment (PLI), high functioning autism (HFA) or specific language impairment (SLI) were compared on measures of social interaction with peers (PI), restricted and repetitive behaviours/interests (RRBIs) and language ability. Odds ratios (OR) from a multinomial logistic regression were used to determine the importance of each measure to diagnostic grouping. MANOVA was used to investigate differences in subscale scores for the PI measure. RESULTS: Greater degrees of PI difficulties (OR = 1.22, 95% CI = 1.05-1.41), RRBI (OR = 1.23, 95% CI = 1.06-1.42) and expressive language ability (OR = 1.16, 95% CI = 1.03-1.30) discriminated HFA from PLI. PLI was differentiated from SLI by elevated PI difficulties (OR = 0.82, 95% CI = 0.70-0.96) and higher expressive language ability (OR = 0.88, 95% CI = 0.77-0.98), but indistinguishable from SLI using RRBI (OR = 1.01, 95% CI=0.94-1.09). A significant effect of group on PI subscales was observed (θ = 1.38, F(4, 56) = 19.26, p < .01) and PLI and HFA groups shared a similar PI subscale profile. CONCLUSIONS: Results provide empirical support for a conceptualisation of PLI as a developmental impairment distinguishable from HFA by absence of RRBIs and by the presence of expressive language difficulties. PI difficulties appear elevated in PLI compared with SLI, but may be less pervasive than in HFA. Findings are discussed with reference to the proposed new category of 'social communication disorder' in DSM-5.

The specificity of notation codes in apraxic agraphia: dissociation between Arabic and alphabetical scripts in a patient with severe ideomotor and visuoconstructional apraxia.

This article describes the case of a patient with corticobasal syndrome, who showed severe ideomotor and visuoconstructional apraxia along with handwriting difficulties more marked for letters and words than for digits and numbers. For alphabetical script, these difficulties were less marked when graphic motor patterns were activated with a model, whilst for digits IV's graphic productions were better in dictation. Moreover, IV's graphic production was negatively influenced by graphomotor complexity for letters but not for numbers. IV is the first reported case of a patient with severe limb apraxia, who also showed peripheral agraphia, with dissociation in alphabetical and numerical notation codes resulting from a specific deficit in the activation of graphomotor programs.

Western Aphasia Battery-Revised Profiles in Primary Progressive Aphasia and Primary Progressive Apraxia of Speech.

Purpose The primary aim was to examine the utility of the Western Aphasia Battery-Revised (WAB-R; Kertesz, 2007) for classifying variants of primary progressive aphasia (PPA). Traditional WAB-R metrics of Aphasia Quotient (AQ), subtest scores, WAB-R classification, and several novel metrics were examined. A secondary aim was to examine these same WAB-R metrics in individuals with primary progressive apraxia of speech (PPAOS). Method A retrospective analysis of WAB-R records from 169 participants enrolled in a study of neurodegenerative speech and language disorders was conducted. PPA/PPAOS classification was determined by consensus review of speech, language, and cognitive profiles. Scores on each of the WAB-R subtests were obtained to derive AQ, WAB-R aphasia profile, and 3 ratios reflecting relative performance on subtests. Results Mean AQ was significantly higher in the PPAOS group compared to all PPA variants except primary fluent aphasia. AQ above the normal cutoff was observed for 20% of participants with PPA. Significant main effects of group were noted for each of the subtests. Follow-up comparisons most frequently discriminated PPAOS, primary agrammatic aphasia (PAA), and logopenic progressive aphasia. Primary fluent aphasia and semantic dementia (SD) subtest scores were less distinctive, with the exception of Naming for SD, which was significantly lower than for PAA and PPAOS. When the WAB-R AQ detected aphasia, a classification of anomic aphasia was most frequently observed; this pattern held true for each of the PPA variants. The mean Information Content:Naming ratio was highest for SD, and the mean Comprehension:Fluency ratio was highest for PAA. Conclusions In the current study, AQ underestimated the presence of PPA and WAB-R classification did not distinguish among PPA classification determined by consensus. Performance on individual subtests and relative performance across subtests demonstrated inconsistent alignment with PPA classification. We conclude the WAB-R in isolation is inadequate to detect or characterize PPA. We instead suggest utilizing the WAB-R as 1 component of a comprehensive language and motor speech assessment when PPA is suspected.

Speech Fluency in Acquired Apraxia of Speech During Narrative Discourse: Group Comparisons and Dual-Task Effects.

Purpose Slowed speech and interruptions to the flow of connected speech are common in aphasia. These features are also observed during dual-task performance for neurotypical adults. The purposes of this study were to determine (a) whether indices of fluency related to cognitive-linguistic versus motor processing would differ between speakers with aphasia plus apraxia of speech (AOS) and speakers with aphasia only and (b) whether cognitive load reduces fluency in speakers with aphasia with and without AOS. Method Fourteen speakers with aphasia (7 with AOS) and 7 neurotypical controls retold short stories alone (single task) and while simultaneously distinguishing between a high and a low tone (dual task). Their narrative samples were analyzed for speech fluency according to sample duration, speech rate, pause/fill time, and repetitions per syllable. Results As expected, both speaker groups with aphasia spoke slower and with more pauses than the neurotypical controls. The speakers with AOS produced more repetitions and longer samples than controls, but they did not differ on these measures from the speakers with aphasia without AOS. Relative to the single-task condition, the dual-task condition increased the duration of pauses and fillers for all groups but reduced speaking rate only for the control group. Sample duration and frequency of repetitions did not change in response to cognitive load. Conclusions Speech output in aphasia becomes less fluent when speakers have to engage in simultaneous tasks, as is typical in everyday conversation. Although AOS may lead to more sound and syllable repetitions than normal, speaking tasks other than narrative discourse might better capture this specific type of disfluency. Future research is needed to confirm and expand these preliminary findings. Supplemental Material https://doi.org/10.23641/asha.8847845.

Interrater Reliability and Concurrent Validity for the Apraxia of Speech Rating Scale 3.0: Application With Persons With Acquired Apraxia of Speech and Aphasia.

Purpose This investigation was designed to provide interrater reliability data for the Apraxia of Speech Rating Scale 3.0 (ASRS 3.0; Strand, Duffy, Clark, & Josephs, 2014 ). Importantly, ratings were completed by investigators who were not involved with the ASRS development. Another aim was to evaluate the relationship of the ASRS 3.0 total score to word intelligibility. Method Two investigators independently completed ASRS 3.0 ratings for 28 participants with chronic apraxia of speech and aphasia. Intelligibility scores were obtained for all participants. Results Consistency of ratings for each feature and total score of the ASRS 3.0 was measured using intraclass correlation coefficients. Twelve of 13 intraclass correlation coefficients for feature ratings reached significance; clinical meaningfulness ranged from poor to excellent. Interrater reliability for the total scores was excellent. Similarly, absolute difference of ratings was minimal for the total scores, but varied across the 13 feature ratings. Correlations between the intelligibility scores and ASRS 3.0 total score were moderate to strong. Conclusion The total ASRS 3.0 score may be viewed as a reliable indicator of prevalence of apraxia of speech features. Although there was good to acceptable correspondence in ratings of the majority of the individual features, additional operationalization of rating procedures may be needed to improve interrater reliability for a few features.

The disconnection apraxias.

Limb apraxia is the loss of the ability to perform voluntary skilled movements, when this loss cannot be attributed to elemental sensorimotor deficits. Successful manual interactions with the objects in the environment require the storage of information about movement parameters. This information is stored in specific cortical modules and the correct performance of a skilled act requires interactions between these modules. Thus, apraxia can occur with degradation of these critical representations or a disconnection between modules. The goal of this paper is to define the different forms of limb apraxia and discuss how apraxia can be induced by both a deterioration of these modules as well as disconnections between these modules that form an anatomically distributed system.

[Diagnosis of developmental dyspraxia].

In the absence of any known neurological condition or intellectual impairment, dyspraxia, also known as developmental coordination disorder, should be considered. Dyspraxia is the inability to plan, organize and execute movements. At all ages, dyspraxia can be congenital or acquired. While some learn to cope with their motor difficulties over the years, the majority will retain them as adults. Children with significant functional impairment should be identified and assessed as early as possible, since failure to address the motor and other commonly associated (co-morbid) features may have major consequences in adult life.

Prosodic and phonetic subtypes of primary progressive apraxia of speech.

Primary progressive apraxia of speech (PPAOS) is a clinical syndrome in which apraxia of speech is the initial indication of neurodegenerative disease. Prior studies of PPAOS have identified hypometabolism, grey matter atrophy, and white matter tract degeneration in the frontal gyri, precentral cortex, and supplementary motor area (SMA). Recent clinical observations suggest two distinct subtypes of PPAOS may exist. Phonetic PPAOS is characterized predominantly by distorted sound substitutions. Prosodic PPAOS is characterized predominantly by slow, segmented speech. Demographic, clinical, and neuroimaging data (MRI, DTI, and FDG-PET) were analyzed to validate these subtypes and explore anatomic correlates. The Phonetic subtype demonstrated bilateral involvement of the SMA, precentral gyrus, and cerebellar crus. The Prosodic subtype demonstrated more focal involvement in the SMA and right superior cerebellar peduncle. The findings provide converging evidence that differences in the reliably determined predominant clinical characteristics of AOS are associated with distinct imaging patterns, independent of severity.

Apraxia: a review.

Praxic functions are frequently altered following brain lesion, giving rise to apraxia - a complex pattern of impairments that is difficult to assess or interpret. In this chapter, we review the current taxonomies of apraxia and related cognitive and neuropsychological models. We also address the questions of the neuroanatomical correlates of apraxia, the relation between apraxia and aphasia and the analysis of apraxic errors. We provide a possible explanation for the difficulties encountered in investigating apraxia and also several approaches to overcome them, such as systematic investigation and modeling studies. Finally, we argue for a multidisciplinary approach. For example, apraxia should be studied in consideration with and could contribute to other fields such as normal motor control, neuroimaging and neurophysiology.

Clinicopathological and imaging correlates of progressive aphasia and apraxia of speech.

Apraxia of speech (AOS) is a motor speech disorder characterized by slow speaking rate, abnormal prosody and distorted sound substitutions, additions, repetitions and prolongations, sometimes accompanied by groping, and trial and error articulatory movements. Although AOS is frequently subsumed under the heading of aphasia, and indeed most often co-occurs with aphasia, it can be the predominant or even the sole manifestation of a degenerative neurological disease. In this study we determine whether the clinical classifications of aphasia and AOS correlated with pathological diagnoses and specific biochemical and anatomical structural abnormalities. Seventeen cases with initial diagnoses of a degenerative aphasia or AOS were re-classified independently by two speech-language pathologists--blinded to pathological and biochemical findings--into one of five operationally defined categories of aphasia and AOS. Pathological diagnoses in the 17 cases were progressive supranuclear palsy in 6, corticobasal degeneration in 5, frontotemporal lobar degeneration with ubiquitin-only-immunoreactive changes in 5 and Pick's disease in 1. Magnetic resonance imaging analysis using voxel-based morphometry (VBM), and single photon emission tomography were completed, blinded to the clinical diagnoses, and clinicoimaging and clinicopathological associations were then sought. Interjudge clinical classification reliability was 87% (kappa = 0.8) for all evaluations. Eleven cases had evidence of AOS, of which all (100%) had a pathological diagnosis characterized by underlying tau biochemistry, while five of the other six cases without AOS did not have tau biochemistry (P = 0.001). A majority of the 17 cases had more than one yearly evaluation, demonstrating the evolution of the speech and language syndromes, as well as motor signs. VBM revealed the premotor and supplemental motor cortices to be the main cortical regions associated with AOS, while the anterior peri-sylvian region was associated with non-fluent aphasia. Refining the classification of the degenerative aphasias and AOS may be necessary to improve our understanding of the relationships among behavioural, pathological and imaging correlations.

[Different patterns of velopharyngeal dysfunction in cleft palate patients]. / Formen der velopharyngealen Dysfunktion bei Spaltpatienten.

BACKGROUND: Velopharyngeal dysfunction (VPD) is generally known to be difficult to influence. Dysfunctional velopharyngeal motor patterns during speech were analyzed with the aim of optimizing the therapeutic strategies. METHODS: Velopharyngeal dysfunctions were videotaped and contextually analyzed during 89 speech sequences in 25 patients. Distinctive features of the motor patterns formed the basis of categorization by three therapists experienced in nasopharyngoscopy. There was a high inter-rater reliability of 94%. RESULTS: A total of four different function profiles were found: 1. VPD with retracted articulatory placement (compensatory articulation) (38%), 2. VPD with motor coordination problems characterized by mistiming of VP movements and voice onset/offset (15%), 3. VPD with verbal dyspraxia characterized by a silent positioning of VP closure before phonation started and a malregulation of muscle tonus (10%) and 4. phoneme-specific VPD (37%). CONCLUSION: Specific knowledge regarding the characteristics of dysfunctional speech motor patterns enables specifically tailored therapy.

A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: I. Development and Description of the Pause Marker.

Purpose: The goal of this article (PM I) is to describe the rationale for and development of the Pause Marker (PM), a single-sign diagnostic marker proposed to discriminate early or persistent childhood apraxia of speech from speech delay. Method: The authors describe and prioritize 7 criteria with which to evaluate the research and clinical utility of a diagnostic marker for childhood apraxia of speech, including evaluation of the present proposal. An overview is given of the Speech Disorders Classification System, including extensions completed in the same approximately 3-year period in which the PM was developed. Results: The finalized Speech Disorders Classification System includes a nosology and cross-classification procedures for childhood and persistent speech disorders and motor speech disorders (Shriberg, Strand, & Mabie, 2017). A PM is developed that provides procedural and scoring information, and citations to papers and technical reports that include audio exemplars of the PM and reference data used to standardize PM scores are provided. Conclusions: The PM described here is an acoustic-aided perceptual sign that quantifies one aspect of speech precision in the linguistic domain of phrasing. This diagnostic marker can be used to discriminate early or persistent childhood apraxia of speech from speech delay.

A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: IV. The Pause Marker Index.

Purpose: Three previous articles provided rationale, methods, and several forms of validity support for a diagnostic marker of childhood apraxia of speech (CAS), termed the pause marker (PM). Goals of the present article were to assess the validity and stability of the PM Index (PMI) to scale CAS severity. Method: PM scores and speech, prosody, and voice precision-stability data were obtained for participants with CAS in idiopathic, neurogenetic, and complex neurodevelopmental disorders; adult-onset apraxia of speech consequent to stroke and primary progressive apraxia; and idiopathic speech delay. Three studies were completed including criterion and concurrent validity studies of the PMI and a temporal stability study of the PMI using retrospective case studies. Results: PM scores were significantly correlated with other signs of CAS precision and stability. The best fit of the distribution of PM scores to index CAS severity was obtained by dividing scores into 4 ordinal severity classifications: mild, mild-moderate, moderate-severe, and severe. Severity findings for the 4 classifications and retrospective longitudinal findings from 8 participants with CAS supported the validity and stability of the PMI. Conclusion: Findings support research and clinical use of the PMI to scale the severity of CAS.

A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: II. Validity Studies of the Pause Marker.

Purpose: The purpose of this 2nd article in this supplement is to report validity support findings for the Pause Marker (PM), a proposed single-sign diagnostic marker of childhood apraxia of speech (CAS). Method: PM scores and additional perceptual and acoustic measures were obtained from 296 participants in cohorts with idiopathic and neurogenetic CAS, adult-onset apraxia of speech and primary progressive apraxia of speech, and idiopathic speech delay. Results: Adjusted for questionable specificity disagreements with a pediatric Mayo Clinic diagnostic standard, the estimated sensitivity and specificity, respectively, of the PM were 86.8% and 100% for the CAS cohort, yielding positive and negative likelihood ratios of 56.45 (95% confidence interval [CI]: [1.15, 2763.31]) and 0.13 (95% CI [0.06, 0.30]). Specificity of the PM for 4 cohorts totaling 205 participants with speech delay was 98.5%. Conclusion: These findings are interpreted as providing support for the PM as a near-conclusive diagnostic marker of CAS.

A Multivariate Analytic Approach to the Differential Diagnosis of Apraxia of Speech.

Purpose: Apraxia of speech (AOS) is a consequence of stroke that frequently co-occurs with aphasia. Its study is limited by difficulties with its perceptual evaluation and dissociation from co-occurring impairments. This study examined the classification accuracy of several acoustic measures for the differential diagnosis of AOS in a sample of stroke survivors. Method: Fifty-seven individuals were included (mean age = 60.8 ± 10.4 years; 21 women, 36 men; mean months poststroke = 54.7 ± 46). Participants were grouped on the basis of speech/language testing as follows: AOS-Aphasia (n = 20), Aphasia Only (n = 24), and Stroke Control (n = 13). Normalized Pairwise Variability Index, proportion of distortion errors, voice onset time variability, and amplitude envelope modulation spectrum variables were obtained from connected speech samples. Measures were analyzed for group differences and entered into a linear discriminant analysis to predict diagnostic classification. Results: Out-of-sample classification accuracy of all measures was over 90%. The envelope modulation spectrum variables had the greatest impact on classification when all measures were analyzed together. Conclusions: This study contributes to efforts to identify objective acoustic measures that can facilitate the differential diagnosis of AOS. Results suggest that further study of these measures is warranted to determine the best predictors of AOS diagnosis. Supplemental Materials: https://doi.org/10.23641/asha.5611309.

Speech apraxia without oral apraxia: can normal brain function explain the physiopathology?

Apraxia of speech, usually associated with stroke, refers to the inability to perform speech motor movements typically with an intact ability to execute non-speech oral movements. It is uncertain whether apraxia of speech results from damage affecting the insula or the inferior frontal gyrus. The controversy started because of conflicting results from studies investigating patients with disrupted brain structure, when dysfunction of both sites can coexist. We conducted a functional magnetic resonance imaging study of individuals without neurological disorders comparing speech and non-speech movements. Speech movements did not recruit the insula, but activated the left inferior frontal gyrus, suggesting that Broca's area, but not the insula, is critical for speech articulation.

Broca's faculté du langage articulé: Language or Praxis?

De Oliveira-Souza, Moll, and Tovar-Moll (this issue) historically reevaluate that Paul Broca's aphemia should be considered as a kind of apraxia rather than aphasia. I argue that such a claim is unwarranted, given the interpretation of the faculty of speech Broca derived from his predecessors, Jean-Baptiste Bouillaud and Franz Joseph Gall, and also with a view on the then generally held opinion that the terms aphémie and aphasie were synonyms. I will discuss evidence that patients such as Leborgne, producing only very few words or syllables, suffer from a global aphasia, affecting all modalities, despite Broca's statement that Leborgne's comprehension was intact. I also point to Broca's claim that the faculty of speech, located in the left anterior hemisphere, is independent from hand preference because it is an intellectual and not a motor function, and to his statement that the cerebral convolutions are not motor organs. I finally contend that, in order to determine whether a given language problem should be labeled as aphasia or apraxia, it is crucial to first be clear on the components of old and new models of language production.