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Apraxia Research Citations

2003 -2004

Acoustic and perceptual correlates of stress in nonwords produced by children with suspected developmental apraxia of speech and children with phonological disorder.
Munson B. Bjorum EM. Windsor J.
Journal of Speech Language & Hearing Research. 46(1):189-202, 2003 Feb.
Abstract

Auditory and phonetic perception of vowels in children with apraxic speech disorders.
Maassen B. Groenen P. & Crul T.
Clinical Linguistics & Phonetics. 17(6):447-67, 2003 Sep.
Abstract

Bilateral brain abnormalities associated with dominantly inherited verbal and orofacial dyspraxia.
Belton E. Salmond CH. Watkins KE. Vargha-Khadem F. & Gadian DG.
Human Brain Mapping. 18(3):194-200, 2003 Mar.
Abstract

Deciphering the genetic basis of speech and language disorders
Fisher SE. Lai CS. & Monaco AP.
Annual Review of Neuroscience.
26:57-80, 2003.
Abstract

Diagnostic assessment of childhood apraxia of speech using automatic speech recognition (ASR) methods.
Hosom, J.P., Shriberg, L., and Green, J.R.
Journal of Medical Speech – Language Pathology
Dec 2004 v12 i4 p167(5)
Abstract

Diagnostic criteria of developmental apraxia of speech used by clinical speech-language pathologists
Forrest, K.
American Journal of Speech-Language Pathology. 12(3):376-80, 2003 Aug.
Abstract

A diagnostic marker for childhood apraxia of speech: the coefficient of variation ratio.
Shriberg LD. Green JR. Campbell TF. McSweeny JL. Scheer AR.
Clinical Linguistics & Phonetics. 17(7):575-95, 2003 Oct-Nov.
Abstract

A diagnostic marker for childhood apraxia of speech: the lexical stress ratio.
Shriberg LD. Campbell TF. Karlsson HB. Brown RL. McSweeny JL. Nadler CJ.
Clinical Linguistics & Phonetics. 17(7):549-74, 2003 Oct-Nov.
Abstract

Evidence of motor programming deficits in children diagnosed with DAS.
Nijland L. Maassen B. & van der Meulen S.
Journal of Speech Language & Hearing Research. 46(2):437-50, 2003 Apr.
Abstract

Family pedigrees of children with suspected childhood apraxia of speech.
Lewis BA, Freebairn LA, Hansen A, Gerry Taylor H, Iyengar S, Shriberg LD.
J Commun Disord. 2004 Mar-Apr;37(2):157-75.
Abstract

FOXP2 expression during brain development coincides with adult sites of pathology in a severe speech and language disorder.
Lai CS. Gerrelli D. Monaco AP. Fisher SE. Copp AJ.
Brain. 126(Pt 11):2455-62, 2003 Nov.
Abstract

Language fMRI abnormalities associated with FOXP2 gene mutation.
Liegeois F. Baldeweg T. Connelly A. Gadian DG. Mishkin M. Vargha-Khadem F.
Nature Neuroscience. 6(11):1230-7, 2003 Nov.
Abstract

Planning of syllables in children with developmental apraxia of speech.
Nijland L. Maassen B. Van Der Meulen S. Gabreels F. Kraaimaat FW. Schreuder R.
Clinical Linguistics & Phonetics. 17(1):1-24, 2003 Jan-Feb.
Abstract

School-age follow-up of children with childhood apraxia of speech.
Lewis BA. Freebairn LA. Hansen AJ. Iyengar SK. Taylor HG.
Language, Speech & Hearing Services in the Schools. 35(2):122-40, 2004
Abstract

Token-to-token variability in developmental apraxia of speech: three longitudinal case studies.
Marquardt TP. Jacks A., & Davis BL.
Clinical Linguistics & Phonetics. 18(2):127-44, 2004 Mar.
Abstract

Verbal dyspraxia and galactosemia.
Webb AL. Singh RH. Kennedy MJ. & Elsas LJ.
Pediatric Research. 53(3):396-402, 2003 Mar.
Abstract

 

Acoustic and perceptual correlates of stress in nonwords produced by children with suspected developmental apraxia of speech and children with phonological disorder.
Munson B. Bjorum EM. Windsor J.
Journal of Speech Language & Hearing Research. 46(1):189-202, 2003 Feb.

Abstract
Previous research (L. Shriberg, D. Aram, & J. Kwiatkowski, 1997b, 1997c) has suggested that accuracy in producing linguistic stress reliably distinguishes between children with suspected developmental apraxia of speech (sDAS) and children with phonological disorder (PD). The current investigation tested this hypothesis by examining acoustic correlates of stress in trochaic (strong-weak) and iambic (weak-strong) nonwords produced by 5 children in each of these 2 groups. Four measures relating to stress production were examined: vowel duration, fundamental frequency(f0) at vowel midpoint, timing of the f0 peak relative to vowel onset, and intensity at vowel midpoint. In addition, perceptual judgments of accuracy of stress production were obtained. No group differences in the production of stress were found; however, listeners judged that the nonword repetitions of children with sDAS matched the target stress contour less often than did the repetitions of children with PD. Multiple regression analyses found that mean vowel duration, as well as the relative duration and relative f0 of stressed and stressless syllables, predicted listeners judgments of stress, although these variables only accounted for a small proportion of variance (21.8%). Thus, children with sDAS were able to produce acoustic differences between stressed tently perceptible to listeners.

 

Auditory and phonetic perception of vowels in children with apraxic speech disorders.
Authors Maassen B. Groenen P. Crul T.
Clinical Linguistics & Phonetics. 17(6):447-67, 2003 Sep.

Abstract
The aim of this study was to assess auditory and phonetic perceptual processing of vowels in children with apraxic disorders, who demonstrated clinically with only a speech output deficit. Two experiments were conducted. In the preparatory Experiment 1 series of vowels were constructed by moving formant frequencies away from the extreme values in the vowel space in the direction of a ‘neutral-vowel position’. These were presented to adults and children with no speech-language involvement. Based on identification performance low-redundancy vowels were selected, which served as the end-points of two vowel continua: /i/-/i/ and /a/-/a/. In Experiment 2 these continua were used in identification and discrimination tasks, presented to 11 children with apraxic speech problems (aged 6:11 to 9:6 years) and 12 normally developing children. The results showed poorer perception of vowels for the children with apraxic speech problems than for the control children for both continua. Identification functions indicated poorer phonetic processing; discrimination functions indicated poorer auditory processing. Furthermore, a combination of perception measures (identification and discrimination) proved to have a high differential and clinical value for the assessment of children with apraxic speech problems. The results support the view that subtle (subclinical) auditory processing deficits make part of speech output disorders.

 

Bilateral brain abnormalities associated with dominantly inherited verbal and orofacial dyspraxia.
Belton E. Salmond CH. Watkins KE. Vargha-Khadem F. Gadian DG.
Human Brain Mapping. 18(3):194-200, 2003 Mar.

Abstract
The KE family is a large three-generational pedigree in which half of the members suffer from a verbal and orofacial dyspraxia in association with a point mutation in the FOXP2 gene. This report extends previous voxel-based morphometric analyses of magnetic resonance imaging (MRI) scans (Watkins et al. [2002] Brain 125:465-478) using a bilateral conjunction analysis. This searches specifically for areas of grey matter density that differ bilaterally in the affected members compared with both matched controls and the unaffected family members. 3-D T1-weighted MRI datasets of 17 family members (10 affected, 7 unaffected) and matched controls were compared. The most significant findings were reduced grey matter density bilaterally in the caudate nucleus, the cerebellum, and the left and right inferior frontal gyrus in the affected members. In addition, increased grey matter density was found bilaterally in the planum temporale. These results confirm that a point mutation in FOXP2 is associated with several bilateral grey matter abnormalities in both motor and language related regions. The results also demonstrate the advantages of using a conjunction analysis when bilateral abnormalities are suspected.

 

Deciphering the genetic basis of speech and language disorders
Fisher SE. Lai CS. Monaco AP.
Annual Review of Neuroscience. 26:57-80, 2003.

Abstract
A significant number of individuals have unexplained difficulties with acquiring normal speech and language, despite adequate intelligence and environmental stimulation. Although developmental disorders of speech and language are heritable, the genetic basis is likely to involve several, possibly many, different risk factors. Investigations of a unique three-generation family showing monogenic inheritance of speech and language deficits led to the isolation of the first such gene on chromosome 7, which encodes a transcription factor known as FOXP2. Disruption of this gene causes a rare severe speech and language disorder but does not appear to be involved in more common forms of language impairment. Recent genome-wide scans have identified at least four chromosomal regions that may harbor genes influencing the latter, on chromosomes 2, 13, 16, and 19. The molecular genetic approach has potential for dissecting neurological pathways underlying speech and language disorders, but such investigations are only just beginning.

 

Diagnostic assessment of childhood apraxia of speech using automatic speech recognition (ASR) methods.
Hosom, J.P., Shriberg, L., and Green, J.R.
Journal of Medical Speech – Language Pathology, Dec 2004 v12 i4 p167(5)

ABSTRACT
We report findings from two feasibility studies using automatic speech recognition (ASR) methods in childhood speech sound disorders. The studies evaluated and implemented the automation of two recently proposed diagnostic markers for suspected apraxia of speech (AOS) termed the Lexical Stress Ratio (LSR) and the Coefficient of Variation Ratio (CVR). The LSR is a weighted composite of amplitude area, frequency area, and duration in the stressed compared to the unstressed vowel as obtained from a speaker’s productions of eight trochaic word forms. Composite weightings for the three stress parameters were determined from a principal components analysis. The CVR expresses the average normalized variability of durations of pause and speech events obtained from a conversational speech sample. We describe the automation procedures used to obtain LSR and CVR scores for four children with suspected AOS and report comparative findings. The LSR values obtained with ASR were within 1.2 to 6.7% of the LSR values obtained manually using Computerized Speech Lab (CSL). The CVR values obtained with ASR were within 0.7 to 2.7% of the CVR values obtained manually using Matlab. These results indicate the potential of ASR-based techniques to process these and other diagnostic markers of childhood speech sound disorders.

 

Diagnostic criteria of developmental apraxia of speech used by clinical speech-language pathologists
Forrest, K.
American Journal of Speech-Language Pathology. 12(3):376-80, 2003 Aug.

Abstract
The diagnostic criteria used to identify developmental apraxia of speech (DAS) have been at the center of controversy for decades. Despite the difficulty in determining the characteristics that differentiate DAS from other speech acquisition disorders, many children are identified with this disorder. The current report presents the criteria used by 75 speech-language pathologists to establish a diagnosis of DAS. Although 50 different characteristics were identified, 6 of these characteristics accounted for 51.5% of the responses. These characteristics included inconsistent productions, general oral-motor difficulties, groping, inability to imitate sounds, increasing difficulty with increased utterance length, and poor sequencing of sounds. These results are consistent with the general ambiguity of the diagnostic criteria of DAS and suggest that no single deficit is used among clinicians.

 

A diagnostic marker for childhood apraxia of speech: the coefficient of variation ratio.
Shriberg LD. Green JR. Campbell TF. McSweeny JL. Scheer AR.
Clinical Linguistics & Phonetics. 17(7):575-95, 2003 Oct-Nov.

Abstract
Terms such as isochrony, syllable segregation, scanning speech and staccato-like rhythmic quality have been used to characterize the temporal regularity that may be a core feature of apraxia of speech. The present report describes a procedure to quantify temporal regularity in children with suspected apraxia of speech (sAOS). Conversational speech samples from 15 such children, together with samples from 30 3-6-year-old children with normal speech acquisition and 30 3-6-year-old children with moderate to severe speech delay of unknown origin, were selected from an audio archive. Signal processing routines were developed to identify and measure the duration of speech and pause events in 24 utterances from the speech samples of each of the 75 speakers. A value termed the coefficient of variation expressed the normalized variability in the durations of each participant’s speech events and pause events within each utterance. A metric termed the coefficient of variation ratio, derived by dividing the coefficient of variation for pause events by the coefficient of variation for speech events, expressed a speaker’s relative temporal variation in the two domains. The 15 children with sAOS had higher coefficient of variation ratios than the 30 children in each of the two comparison groups, indicating that the children with sAOS had proportionally more variation in the duration of pause events and/or less variation in the duration of speech events. Findings are interpreted as supporting the view that a constraint in speech timing is a core feature of the praxis disorder that defines a developmental form of apraxia of speech.

 

A diagnostic marker for childhood apraxia of speech: the lexical stress ratio.
Shriberg LD. Campbell TF. Karlsson HB. Brown RL. McSweeny JL. Nadler CJ.
Clinical Linguistics & Phonetics. 17(7):549-74, 2003 Oct-Nov.

Abstract
This report includes an extended review of the contemporary inclusionary criteria used to identify children with suspected apraxia of speech (sAOS) and describes findings supporting a lexical stress marker for sAOS. The thesis is that although a deficit in speech praxis is the core disorder in sAOS, only a few diagnostic markers for sAOS assess this speech motor control construct. The proposed marker is a composite lexical stress ratio (LSR) that quantifies the acoustic correlates of stress (frequency, intensity, duration) in bisyllabic word forms. Responses to a lexical stress task were obtained from 35 participants referred for a study of apraxia of speech. Eleven of the children were classified as sAOS, because they met one or both of two investigator groups’ provisional criteria for sAOS. The 24 remaining children who did not meet either group’s criteria were classified as having speech delay (SD). The first question posed was whether the LSR scores of children with sAOS differed from those of children with SD. Findings were affirmative. Of the six LSRs at the upper and lower extremes of the obtained distributions of LSR scores (approximately 8% of scores at each end), five (83%) were from speakers with sAOS (p < 0.003). The second question was whether findings for the sAOS speakers were more consistent with deficits in speech motor control or with deficits in underlying phonological representational aspects of lexical stress. A parsimonious interpretation of the present findings, together with findings from other studies, suggests that they reflect the prosodic consequences of a praxis deficit in speech motor control.

 

Evidence of motor programming deficits in children diagnosed with DAS.
Nijland L. Maassen B. van der Meulen S.
Journal of Speech Language & Hearing Research. 46(2):437-50, 2003 Apr.

Abstract
In this study the hypothesis of motor programming involvement in developmental apraxia of speech (DAS) was investigated by studying articulatory compensation. Five children with DAS and 5 normally speaking children (age 5;0[years;months] to 6;10), and 6 adult women produced utterances in a normal speaking condition and in a bite-block condition in which the mandible was kept in a fixed position. Throughout the utterances, the course of the second formant was used to determine articulatory compensation and the effect of the bite block on anticipatory coarticulation. Results showed that the bite-block condition in normally speaking children, like in adult women, did not affect the extent of anticipatory coarticulation. In the speech of children with DAS, the bite block had large effects on coarticulatory patterns and on vowel quality, which, contrary to expectations, had improved. These results are interpreted as a clear demonstration of deficient motor programming in DAS.

 

Family pedigrees of children with suspected childhood apraxia of speech.
Lewis BA, Freebairn LA, Hansen A, Gerry Taylor H, Iyengar S, Shriberg LD.
J Commun Disord. 2004 Mar-Apr;37(2):157-75.

Abstract
Forty-two children (29 boys and 13 girls), ages 3-10 years, were referred from the caseloads of clinical speech-language pathologists for suspected childhood apraxia of speech (CAS). According to results from tests of speech and oral motor skills, 22 children met criteria for CAS, including a severely limited consonant and vowel repertoire, difficulty sequencing syllables, and inconsistent and unusual errors. Family pedigrees for these children were constructed through parent interviews and direct testing of nuclear family members. Familial aggregation for speech-sound and language disorders was demonstrated with 86% reporting at least one nuclear family member affected. Based on parent report, 13 of the 22 children (59%) had at least one affected parent. However, CAS was evident in only two siblings of probands with CAS and two probands with other speech-sound disorders. Based on testing, overall affection rates of speech-sound/language disorders were higher in families of children with CAS than in families of children with other speech-sound disorders. Mothers of children with CAS demonstrated a higher affection rate than mothers of children with other speech-sound disorders. A sex-related threshold model of transmission was also supported with brothers more often affected than sisters for male probands only. If our inclusionary criteria for CAS are valid, these findings support a general verbal trait deficit hypothesis.

 

FOXP2 expression during brain development coincides with adult sites of pathology in a severe speech and language disorder.
Lai CS. Gerrelli D. Monaco AP. Fisher SE. Copp AJ.
Brain. 126(Pt 11):2455-62, 2003 Nov.

Abstract
Disruption of FOXP2, a gene encoding a forkhead-domain transcription factor, causes a severe developmental disorder of verbal communication, involving profound articulation deficits, accompanied by linguistic and grammatical impairments. Investigation of the neural basis of this disorder has been limited previously to neuroimaging of affected children and adults. The discovery of the gene responsible, FOXP2, offers a unique opportunity to explore the relevant neural mechanisms from a molecular perspective. In the present study, we have determined the detailed spatial and temporal expression pattern of FOXP2 mRNA in the developing brain of mouse and human. We find expression in several structures including the cortical plate, basal ganglia, thalamus, inferior olives and cerebellum. These data support a role for FOXP2 in the development of corticostriatal and olivocerebellar circuits involved in motor control. We find intriguing concordance between regions of early expression and later sites of pathology suggested by neuroimaging. Moreover, the homologous pattern of FOXP2/Foxp2 expression in human and mouse argues for a role for this gene in development of motor-related circuits throughout mammalian species. Overall, this study provides support for the hypothesis that impairments in sequencing of movement and procedural learning might be central to the FOXP2-related speech and language disorder.

 

Language fMRI abnormalities associated with FOXP2 gene mutation.
Liegeois F. Baldeweg T. Connelly A. Gadian DG. Mishkin M. Vargha-Khadem F.
Nature Neuroscience. 6(11):1230-7, 2003 Nov.

Abstract
Half the members of the KE family suffer from a speech and language disorder caused by a mutation in the FOXP2 gene. We examined functional brain abnormalities associated with this mutation using two fMRI language experiments, one involving covert (silent) verb generation and the other overt (spoken) verb generation and word repetition. The unaffected family members showed a typical left-dominant distribution of activation involving Broca’s area in the generation tasks and a more bilateral distribution in the repetition task, whereas the affected members showed a more posterior and more extensively bilateral pattern of activation in all tasks. Consistent with previously reported bilateral morphological abnormalities, the affected members showed significant underactivation relative to the unaffected members in Broca’s area and its right homolog, as well as in other cortical language-related regions and in the putamen. Our findings suggest that the FOXP2 gene is critically involved in the development of the neural systems that mediate speech and language.

 

Planning of syllables in children with developmental apraxia of speech.
Nijland L. Maassen B. Van Der Meulen S. Gabreels F. Kraaimaat FW. Schreuder R.
Clinical Linguistics & Phonetics. 17(1):1-24, 2003 Jan-Feb.

Abstract
The aim of the present study was to investigate whether children with developmental apraxia of speech (DAS) show a deficit in planning syllables in speech production. Six children with DAS and six normally speaking (NS) children produced high- and low-frequency of occurrence syllable utterances, in which the syllable structure was systematically manipulated in an otherwise unchanging phoneme sequence. Anticipatory coarticulation, using second formant trajectories, and durational structure were analysed. The results showed stronger coarticulation in the children with DAS when compared to the normally speaking children. but in contrast to our expectations, in neither group was a systematic effect of syllable structure on the second format trajectory found. Effects of syllable structure did emerge for durational structure in that durational adjustments were found in the segments of the second syllable. These adjustments were less systematic in children with DAS when compared to normally speaking children. Furthermore, at the prosodic level, normally speaking children showed metrical contrasts that were not realized by the children with DAS. The latter results are interpreted as evidence for a problem in the planning of syllables in speech production of children with DAS, in particular concerning prosodic aspects, which is discussed in relation to the automation of speech production.

 

School-age follow-up of children with childhood apraxia of speech.
Lewis BA. Freebairn LA. Hansen AJ. Iyengar SK. Taylor HG.
Language, Speech & Hearing Services in the Schools. 35(2):122-40, 2004

Abstract:
PURPOSE: The primary aim of this study was to examine differences in speech/language and written language skills between children with suspected childhood apraxia of speech (CAS) and children with other speech-sound disorders at school age.
METHOD: Ten children (7 males and 3 females) who were clinically diagnosed with CAS (CAS group) were followed from the preschool years (ages 4-6) to school age (ages 8-10) and were compared with children with isolated speech-sound disorders (S group; n = 15) and combined speech-sound and language disorders (SL group; n = 14). Assessments included measures of articulation, diadochokinetic rates, language, reading, and spelling.
RESULTS: At follow-up, 8 of the children with CAS demonstrated improvement in articulation scores, but all 10 continued to have difficulties in syllable sequencing, nonsense word repetition, and language abilities. The children also exhibited comorbid disorders of reading and spelling. Group comparisons revealed that the CAS group was similar to the SL group, but not the S group during the preschool years. By school age, however, the SL group made more positive changes in language skills than the CAS group. CLINICAL IMPLICATIONS: These findings suggest that the phenotype for CAS changes with age. Language disorders persist in these children despite partial resolution of articulation problems. Children with CAS are also at risk for reading and spelling problems.

 

Token-to-token variability in developmental apraxia of speech: three longitudinal case studies.
Marquardt TP. Jacks A. Davis BL.
Clinical Linguistics & Phonetics. 18(2):127-44, 2004 Mar.

Abstract
Variability in the speech production patterns of children with developmental apraxia of speech (DAS) was investigated in a three-year longitudinal study of three children with DAS. A metric was developed to measure token-to-token variability in repeated word productions from connected speech samples. Results suggest that high levels of total token and error token variability and low levels of word target stability and token accuracy characterize the disorder. Overall levels of variability and patterns of change over time differed between participants. Longitudinal patterns were indicative of decreasing total token variability and increasing token accuracy. However, change was not consistently unidirectional for two of the three children in the study, suggesting day-to-day performance differences in addition to within-session variability.

 

Verbal dyspraxia and galactosemia.
Webb AL. Singh RH. Kennedy MJ. Elsas LJ.
Pediatric Research. 53(3):396-402, 2003 Mar.

Abstract
Classical galactosemia is an autosomal recessive disorder resulting from deficient galactose-1-phosphateuridyl transferase (GALT) activity. Verbal dyspraxia is an unusual outcome in galactosemia. Here we validated a simplified breath test of total body galactose oxidation against genotype and evaluated five potential biochemical risk indicators for verbal dyspraxia in galactosemia: cumulative percentage dose (CUMPCD) of (13)CO(2) in breath, mean erythrocyte galactose-1-phosphate, highest erythrocyte galactose-1-phosphate, mean urinary galactitol, and erythrocyte GALT activity. Thirteen controls and 42 patients with galactosemia took a (13)C-galactose bolus, and the (CUMPCD) of (13 CO(2) in expired air was determined. Patients with or =5% CUMPCD had milder mutant human GALT alleles. Twenty-four patients consented to formal speech evaluation; 15 (63%) had verbal dyspraxia. Dyspraxic patients had significantly lower CUMPCD values (2.84 +/- 5.76% versus 11.51 +/- 7.67%; p < 0.008) and significantly higher mean erythrocyte galactose-1-phosphate (3.38 +/- 0.922 mg/dL versus 1.92 +/- 1.28 mg/dL; p = 0.019) and mean urinary galactitol concentrations (192.4 +/- 75.8 mmol/mol creatinine versus 122.0 +/- 56.4; p = 0.048) than patients with normal speech. CUMPCD values2.7 mg/dL, and mean urinary galactitol levels >135 mmol/mol creatinine were associated with dyspraxic outcome with odds ratios of 21, 13, and 5, respectively. We conclude that total body oxidation of galactose to CO(2) in expired air reflects genotype and that this breath test is a sensitive predictor of verbal dyspraxia in patients with galactosemia.