Speech entrainment enables patients with Broca's aphasia to produce fluent speech
Speech entrainment enables patients with Broca's aphasia to produce fluent speech
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DOI：
10.1093/brain/aws301
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发表时间：
2012-12-01
期刊：
影响因子：
14.5
通讯作者：
Rorden, Chris
中科院分区：
文献类型：
--
作者：
Fridriksson, Julius;Hubbard, H. Isabel;Rorden, Chris
布罗卡失语症的一个显著特征是不流利的停顿性言语，通常每句话涉及一到三个词。然而，尽管有如此严重的损伤，一些患者可以模仿视听言语刺激，使他们能够在真实的时间内产生流利的言语。我们称这种效应为“言语诱导”，并揭示其神经机制，以及探索其作为治疗布罗卡失语症的言语产生的有用性。在实验1中，13例布洛卡失语症患者在三种情况下进行了测试：（i）语音夹带与视听反馈，他们试图模仿扬声器的嘴被认为是在iPod屏幕上;（ii）语音夹带与音频唯一的反馈，患者模仿听到的讲话;和（iii）自发的讲话，患者自由地谈论指定的主题。患者产生了更大的各种各样的话，使用视听反馈相比，只有音频反馈和自发的讲话。在纯音频反馈和自发言语之间没有发现差异。在实验2中，实验1中的13名患者中的10名和20名对照受试者进行了功能性磁共振成像，以确定支持语音夹带的神经机制。患者和对照组的结果显示，与自发性语音相比，在前额叶和Brodmann区47的交界处，Brodmann区37，以及左侧颞中回和Broca区背侧部分的单侧，在语音夹带期间产生的语音双侧皮层激活更大。在正常受试者中为这些区域构建的可能的白色物质束揭示了通过胼胝体和腹侧纤维通过末端囊连接的结构网络。单侧区域通过弓状束连接。在实验3中，实验1中包括的所有患者都参加了为期6周的治疗阶段，使用语音诱导来改善语音产生。在治疗阶段之前和之后收集行为和功能磁共振成像数据。在训练后1周和6周，患者能够产生更多种类的单词，有和没有语音夹带。在左后下顶叶区域发现了与语音夹带相关的皮质激活的给药相关降低。我们的结论是，语音夹带允许患者与布洛卡失语症，以增加一倍，他们的语音输出相比，自发的讲话。神经影像学结果表明，语音夹带允许患者通过提供外部门控机制，轭腹侧语言网络，编码语音的概念方面产生流利的语音。初步结果表明，语音夹带的培训提高了布罗卡失语症的语音生产提供了一个潜在的治疗方法，已被证明是特别耐治疗的疾病。
A distinguishing feature of Broca's aphasia is non-fluent halting speech typically involving one to three words per utterance. Yet, despite such profound impairments, some patients can mimic audio-visual speech stimuli enabling them to produce fluent speech in real time. We call this effect 'speech entrainment' and reveal its neural mechanism as well as explore its usefulness as a treatment for speech production in Broca's aphasia. In Experiment 1, 13 patients with Broca's aphasia were tested in three conditions: (i) speech entrainment with audio-visual feedback where they attempted to mimic a speaker whose mouth was seen on an iPod screen; (ii) speech entrainment with audio-only feedback where patients mimicked heard speech; and (iii) spontaneous speech where patients spoke freely about assigned topics. The patients produced a greater variety of words using audio-visual feedback compared with audio-only feedback and spontaneous speech. No difference was found between audio-only feedback and spontaneous speech. In Experiment 2, 10 of the 13 patients included in Experiment 1 and 20 control subjects underwent functional magnetic resonance imaging to determine the neural mechanism that supports speech entrainment. Group results with patients and controls revealed greater bilateral cortical activation for speech produced during speech entrainment compared with spontaneous speech at the junction of the anterior insula and Brodmann area 47, in Brodmann area 37, and unilaterally in the left middle temporal gyrus and the dorsal portion of Broca's area. Probabilistic white matter tracts constructed for these regions in the normal subjects revealed a structural network connected via the corpus callosum and ventral fibres through the extreme capsule. Unilateral areas were connected via the arcuate fasciculus. In Experiment 3, all patients included in Experiment 1 participated in a 6-week treatment phase using speech entrainment to improve speech production. Behavioural and functional magnetic resonance imaging data were collected before and after the treatment phase. Patients were able to produce a greater variety of words with and without speech entrainment at 1 and 6 weeks after training. Treatment-related decrease in cortical activation associated with speech entrainment was found in areas of the left posterior-inferior parietal lobe. We conclude that speech entrainment allows patients with Broca's aphasia to double their speech output compared with spontaneous speech. Neuroimaging results suggest that speech entrainment allows patients to produce fluent speech by providing an external gating mechanism that yokes a ventral language network that encodes conceptual aspects of speech. Preliminary results suggest that training with speech entrainment improves speech production in Broca's aphasia providing a potential therapeutic method for a disorder that has been shown to be particularly resistant to treatment.