Speech profiles and cue responsiveness in primary progressive aphasia

摘要 建议研究的目的是加强当前项目对语音的影响 左半球卒中后的曲线（R 01 DC 018569）。具体而言，我们寻求扩大其范围， 原发性进行性失语，见于额颞叶变性的某些表型， 老年痴呆症位于查佩尔山的北卡罗来纳州大学最近的研究表明， 在中风诱发的失语症中展示了一系列定量语言特征。这些配置文件 包括语言失用症--一种运动编程障碍， 用传统的感知方法进行诊断。虽然言语失用症通常是由中风引起的， 也发生在退行性疾病中，其存在或不存在是行为的核心。 原发性进行性失语的变异之间的分化，并预测潜在的 病理学1，2.因此，诊断是必不可少的早期诊断和治疗。通过 与德克萨斯大学奥斯汀分校和新墨西哥州大学的同事合作， 我们计划应用父中风项目的实验条件和分析程序， 患有原发性进行性失语症的人。我们预计，这一扩张将促进协同 跨不同病理的神经行为研究，影响重叠的大脑区域， 网络.在目标1中，我们将评估我们正在开发的语音评估的程度 中风诱发的言语失用症适用于原发性进行性失语。我们计划调整 参数，以确保心理测量的严谨性和两种病因的临床可行性。 预期的工具和程序将是有价值的所有研究人员和临床医生的工作涉及 这些临床人群中的任何一个。在目标2中，我们将确定言语失用症的程度， 相关的言语特征预测对行为提示策略的反应。通过复制 实验条件中使用的中风为重点的父母补助金，我们将有助于收敛 不同左半球后认知补偿和学习能力的证据 病理结合母项目，这两个目标将为以下方面奠定基础： 超越传统障碍病因学界限的合作研究。

ABSTRACT The purpose of the proposed research is to strengthen the impact of a current project on speech profiles after left hemisphere stroke (R01DC018569). Specifically, we seek to expand its scope to primary progressive aphasia as seen in some phenotypes of frontotemporal lobar degeneration and Alzheimer’s disease. Recent research at The University of North Carolina at Chapel Hill has demonstrated a spectrum of quantitative speech profiles in stroke-induced aphasia. These profiles include apraxia of speech—a disorder of motor programming that has been notoriously difficult to diagnose with traditional perceptual methods. Though apraxia of speech is usually caused by stroke, it also occurs in degenerative disease, where its presence or absence is central to the behavioral differentiation among variants of primary progressive aphasia and is predictive of underlying pathology1,2. As such, the diagnosis is essential to early prognostication and treatment. Through collaboration with colleagues at The University of Texas at Austin and The University of New Mexico, we plan to apply experimental conditions and analysis procedures from the parent stroke project to persons with primary progressive aphasia. We expect this expansion will facilitate synergistic neurobehavioral research across distinct pathologies that affect overlapping brain regions and networks. In Aim 1 we will evaluate the extent to which the speech assessment we are developing for stroke-induced apraxia of speech is applicable to primary progressive aphasia. We plan to adjust parameters as needed to ensure psychometric rigor and clinical feasibility for both etiologies. Anticipated tools and procedures will be of value to all researchers and clinicians whose work involves either of these clinical populations. In Aim 2, we will determine to what extent apraxia of speech and related speech profiles predict responsiveness to behavioral cueing strategies. By replicating experimental conditions utilized in the stroke-focused parent grant, we will contribute to converging evidence about cognitive compensation and capacity for learning after diverse left hemisphere pathology. In conjunction with the parent project, these two aims will establish a foundation for collaborative research beyond traditional boundaries of disorder etiology.