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1.  Behavioral, computational, and neuroimaging studies of acquired apraxia of speech 
A critical examination of speech motor control depends on an in-depth understanding of network connectivity associated with Brodmann areas 44 and 45 and surrounding cortices. Damage to these areas has been associated with two conditions—the speech motor programming disorder apraxia of speech (AOS) and the linguistic/grammatical disorder of Broca’s aphasia. Here we focus on AOS, which is most commonly associated with damage to posterior Broca’s area (BA) and adjacent cortex. We provide an overview of our own studies into the nature of AOS, including behavioral and neuroimaging methods, to explore components of the speech motor network that are associated with normal and disordered speech motor programming in AOS. Behavioral, neuroimaging, and computational modeling studies are indicating that AOS is associated with impairment in learning feedforward models and/or implementing feedback mechanisms and with the functional contribution of BA6. While functional connectivity methods are not yet routinely applied to the study of AOS, we highlight the need for focusing on the functional impact of localized lesions throughout the speech network, as well as larger scale comparative studies to distinguish the unique behavioral and neurological signature of AOS. By coupling these methods with neural network models, we have a powerful set of tools to improve our understanding of the neural mechanisms that underlie AOS, and speech production generally.
doi:10.3389/fnhum.2014.00892
PMCID: PMC4217373  PMID: 25404911
apraxia of speech; speech motor control; DIVA; feedforward control; feedback control; inferior frontal gyrus (IFG); premotor cortex
2.  Altered resting-state network connectivity in stroke patients with and without apraxia of speech 
NeuroImage : Clinical  2015;8:429-439.
Motor speech disorders, including apraxia of speech (AOS), account for over 50% of the communication disorders following stroke. Given its prevalence and impact, and the need to understand its neural mechanisms, we used resting state functional MRI to examine functional connectivity within a network of regions previously hypothesized as being associated with AOS (bilateral anterior insula (aINS), inferior frontal gyrus (IFG), and ventral premotor cortex (PM)) in a group of 32 left hemisphere stroke patients and 18 healthy, age-matched controls. Two expert clinicians rated severity of AOS, dysarthria and nonverbal oral apraxia of the patients. Fifteen individuals were categorized as AOS and 17 were AOS-absent. Comparison of connectivity in patients with and without AOS demonstrated that AOS patients had reduced connectivity between bilateral PM, and this reduction correlated with the severity of AOS impairment. In addition, AOS patients had negative connectivity between the left PM and right aINS and this effect decreased with increasing severity of non-verbal oral apraxia. These results highlight left PM involvement in AOS, begin to differentiate its neural mechanisms from those of other motor impairments following stroke, and help inform us of the neural mechanisms driving differences in speech motor planning and programming impairment following stroke.
Highlights
•Resting state fMRI connectivity of a speech network in apraxia of speech (AOS)•AOS patients had reduced bilateral premotor (PM) connectivity relative to severity.•AOS patients also had reduced left PM–right anterior insula connectivity.•Left PM may drive disordered speech motor planning and programming post-stroke.
doi:10.1016/j.nicl.2015.03.013
PMCID: PMC4473263  PMID: 26106568
Apraxia of speech; Network connectivity; Resting-state fMRI; Stroke
3.  Logopenic and Nonfluent Variants of Primary Progressive Aphasia Are Differentiated by Acoustic Measures of Speech Production 
PLoS ONE  2014;9(2):e89864.
Differentiation of logopenic (lvPPA) and nonfluent/agrammatic (nfvPPA) variants of Primary Progressive Aphasia is important yet remains challenging since it hinges on expert based evaluation of speech and language production. In this study acoustic measures of speech in conjunction with voxel-based morphometry were used to determine the success of the measures as an adjunct to diagnosis and to explore the neural basis of apraxia of speech in nfvPPA. Forty-one patients (21 lvPPA, 20 nfvPPA) were recruited from a consecutive sample with suspected frontotemporal dementia. Patients were diagnosed using the current gold-standard of expert perceptual judgment, based on presence/absence of particular speech features during speaking tasks. Seventeen healthy age-matched adults served as controls. MRI scans were available for 11 control and 37 PPA cases; 23 of the PPA cases underwent amyloid ligand PET imaging. Measures, corresponding to perceptual features of apraxia of speech, were periods of silence during reading and relative vowel duration and intensity in polysyllable word repetition. Discriminant function analyses revealed that a measure of relative vowel duration differentiated nfvPPA cases from both control and lvPPA cases (r2 = 0.47) with 88% agreement with expert judgment of presence of apraxia of speech in nfvPPA cases. VBM analysis showed that relative vowel duration covaried with grey matter intensity in areas critical for speech motor planning and programming: precentral gyrus, supplementary motor area and inferior frontal gyrus bilaterally, only affected in the nfvPPA group. This bilateral involvement of frontal speech networks in nfvPPA potentially affects access to compensatory mechanisms involving right hemisphere homologues. Measures of silences during reading also discriminated the PPA and control groups, but did not increase predictive accuracy. Findings suggest that a measure of relative vowel duration from of a polysyllable word repetition task may be sufficient for detecting most cases of apraxia of speech and distinguishing between nfvPPA and lvPPA.
doi:10.1371/journal.pone.0089864
PMCID: PMC3938536  PMID: 24587083
4.  A comparison of two treatments for childhood apraxia of speech: methods and treatment protocol for a parallel group randomised control trial 
BMC Pediatrics  2012;12:112.
Background
Childhood Apraxia of Speech is an impairment of speech motor planning that manifests as difficulty producing the sounds (articulation) and melody (prosody) of speech. These difficulties may persist through life and are detrimental to academic, social, and vocational development. A number of published single subject and case series studies of speech treatments are available. There are currently no randomised control trials or other well designed group trials available to guide clinical practice.
Methods/Design
A parallel group, fixed size randomised control trial will be conducted in Sydney, Australia to determine the efficacy of two treatments for Childhood Apraxia of Speech: 1) Rapid Syllable Transition Treatment and the 2) Nuffield Dyspraxia Programme – Third edition. Eligible children will be English speaking, aged 4–12 years with a diagnosis of suspected CAS, normal or adjusted hearing and vision, and no comprehension difficulties or other developmental diagnoses. At least 20 children will be randomised to receive one of the two treatments in parallel. Treatments will be delivered by trained and supervised speech pathology clinicians using operationalised manuals. Treatment will be administered in 1-hour sessions, 4 times per week for 3 weeks. The primary outcomes are speech sound and prosodic accuracy on a customised 292 item probe and the Diagnostic Evaluation of Articulation and Phonology inconsistency subtest administered prior to treatment and 1 week, 1 month and 4 months post-treatment. All post assessments will be completed by blinded assessors. Our hypotheses are: 1) treatment effects at 1 week post will be similar for both treatments, 2) maintenance of treatment effects at 1 and 4 months post will be greater for Rapid Syllable Transition Treatment than Nuffield Dyspraxia Programme treatment, and 3) generalisation of treatment effects to untrained related speech behaviours will be greater for Rapid Syllable Transition Treatment than Nuffield Dyspraxia Programme treatment. This protocol was approved by the Human Research Ethics Committee, University of Sydney (#12924).
Discussion
This will be the first randomised control trial to test treatment for CAS. It will be valuable for clinical decision-making and providing evidence-based services for children with CAS.
Trial Registration
Australian New Zealand Clinical Trials Registry: ACTRN12612000744853
doi:10.1186/1471-2431-12-112
PMCID: PMC3441276  PMID: 22863021
Childhood apraxia of speech; Treatment; Effectiveness; Randomised control trial; Intervention; Rapid syllable transition treatment; Nuffield dyspraxia programme
5.  Neural control of the lips differs for young and older adults following a perturbation 
Aging impairs the control of many skilled movements including speech. The purpose of this paper was to investigate whether young and older adults adapt to lower lip perturbations during speech differently. Twenty men (10 young, 26 ± 3 years of age; 10 older, 60 ± 9 years of age) were requested to repeat the word (“papa”) 300 times. In 15% of the trials, the subjects experienced a mechanical perturbation on the lower lip. Displacement and neural activation (EMG) of the upper and lower lips were evaluated. Perturbations to the lower lip caused a greater increase in the maximum displacement of the lower lip for older adults compared with young adults (34.7 ± 19% vs. 13.4 ± 17%; P = 0.017). Furthermore, young adults exhibited significantly greater 30–100 Hz normalized EMG power for the lower lip compared to the upper lip (P < 0.005). In young adults, changes from normal to perturbed trials in the 30–50 Hz frequency band of the EMG were negatively correlated to the changes from normal to perturbed trials in the lower lip maximum displacement (R2 = 0.48; P = 0.025). It is concluded that young adults adapt better to lower lip perturbations compared with older adults and that the associated neural activation strategy of the involved muscle is different for the two age groups.
doi:10.1007/s00221-010-2411-3
PMCID: PMC3167083  PMID: 20852991
EMG; Wavelet analysis; Speech; Cortical drive

Results 1-5 (5)