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

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          Abstract

          <div class="section"> <a class="named-anchor" id="d1010208e215"> <!-- named anchor --> </a> <h5 class="section-title" id="d1010208e216">Purpose</h5> <p id="d1010208e218">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. </p> </div><div class="section"> <a class="named-anchor" id="d1010208e220"> <!-- named anchor --> </a> <h5 class="section-title" id="d1010208e221">Method</h5> <p id="d1010208e223">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. </p> </div><div class="section"> <a class="named-anchor" id="d1010208e225"> <!-- named anchor --> </a> <h5 class="section-title" id="d1010208e226">Results</h5> <p id="d1010208e228">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. </p> </div><div class="section"> <a class="named-anchor" id="d1010208e230"> <!-- named anchor --> </a> <h5 class="section-title" id="d1010208e231">Conclusion</h5> <p id="d1010208e233">Findings support research and clinical use of the PMI to scale the severity of CAS.</p> </div>

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          Speech Production as State Feedback Control

          Spoken language exists because of a remarkable neural process. Inside a speaker's brain, an intended message gives rise to neural signals activating the muscles of the vocal tract. The process is remarkable because these muscles are activated in just the right way that the vocal tract produces sounds a listener understands as the intended message. What is the best approach to understanding the neural substrate of this crucial motor control process? One of the key recent modeling developments in neuroscience has been the use of state feedback control (SFC) theory to explain the role of the CNS in motor control. SFC postulates that the CNS controls motor output by (1) estimating the current dynamic state of the thing (e.g., arm) being controlled, and (2) generating controls based on this estimated state. SFC has successfully predicted a great range of non-speech motor phenomena, but as yet has not received attention in the speech motor control community. Here, we review some of the key characteristics of speech motor control and what they say about the role of the CNS in the process. We then discuss prior efforts to model the role of CNS in speech motor control, and argue that these models have inherent limitations – limitations that are overcome by an SFC model of speech motor control which we describe. We conclude by discussing a plausible neural substrate of our model.
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            Laryngeal motor cortex and control of speech in humans.

            Speech production is one of the most complex and rapid motor behaviors, and it involves a precise coordination of more than 100 laryngeal, orofacial, and respiratory muscles. Yet we lack a complete understanding of laryngeal motor cortical control during production of speech and other voluntary laryngeal behaviors. In recent years, a number of studies have confirmed the laryngeal motor cortical representation in humans and have provided some information about its interactions with other cortical and subcortical regions that are principally involved in vocal motor control of speech production. In this review, the authors discuss the organization of the peripheral and central laryngeal control based on neuroimaging and electrical stimulation studies in humans and neuroanatomical tracing studies in nonhuman primates. It is hypothesized that the location of the laryngeal motor cortex in the primary motor cortex and its direct connections with the brain stem laryngeal motoneurons in humans, as opposed to its location in the premotor cortex with only indirect connections to the laryngeal motoneurons in nonhuman primates, may represent one of the major evolutionary developments in humans toward the ability to speak and vocalize voluntarily.
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              Computational modeling of stuttering caused by impairments in a basal ganglia thalamo-cortical circuit involved in syllable selection and initiation.

              Atypical white-matter integrity and elevated dopamine levels have been reported for individuals who stutter. We investigated how such abnormalities may lead to speech dysfluencies due to their effects on a syllable-sequencing circuit that consists of basal ganglia (BG), thalamus, and left ventral premotor cortex (vPMC). "Neurally impaired" versions of the neurocomputational speech production model GODIVA were utilized to test two hypotheses: (1) that white-matter abnormalities disturb the circuit via corticostriatal projections carrying copies of executed motor commands and (2) that dopaminergic abnormalities disturb the circuit via the striatum. Simulation results support both hypotheses: in both scenarios, the neural abnormalities delay readout of the next syllable's motor program, leading to dysfluency. The results also account for brain imaging findings during dysfluent speech. It is concluded that each of the two abnormality types can cause stuttering moments, probably by affecting the same BG-thalamus-vPMC circuit. Copyright © 2013 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal of Speech, Language, and Hearing Research
                J Speech Lang Hear Res
                American Speech Language Hearing Association
                1092-4388
                1558-9102
                April 14 2017
                April 14 2017
                : 60
                : 4
                Affiliations
                [1 ]Waisman Center, University of Wisconsin–Madison
                [2 ]Department of Neurology, Mayo Clinic–Rochester, NY
                [3 ]Department of Communication Sciences and Disorders, Augustana College, Rock Island, IL
                Article
                10.1044/2016_JSLHR-S-16-0149
                5548089
                28384662
                e7a94f40-b614-4fd2-a9fc-e817b1cee4ec
                © 2017
                History

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