2013年1月16日 訊 /生物谷BIOON/ --近日,，來自南卡羅來納大學(xué)公共衛(wèi)生學(xué)院的研究者通過研究開發(fā)出了一種“言語誘導(dǎo)”（speech entrainment）的新技術(shù),，這種新技術(shù)可以改善中風(fēng)患者由于患布羅卡氏失語癥所引發(fā)的言語缺失功能,，使患者可以流利地進行講話，相關(guān)研究刊登于國際雜志Brain上,。
失語癥是一種由于大腦左半球損傷而引發(fā)的嚴(yán)重的交流問題,，主要表現(xiàn)為說話時斷時續(xù)，通常在三分之一的中風(fēng)患者中發(fā)生,，嚴(yán)重影響個人的交流溝通能力,。使用這項新技術(shù)可以幫助患者明顯改善其講話的能力。
研究者Julius Fridriksson表示,，我們這項研究首次實現(xiàn)了布羅卡氏失語癥患者可以進行流利地語句交流,，同時這項研究也幫助我們更深入地理解中風(fēng)后患者的大腦功能表現(xiàn)，也為相應(yīng)療法的開發(fā)提供了幫助,。
研究中,，13個患者完成了3組單獨的行為任務(wù)用于理解患者發(fā)聲的轉(zhuǎn)換和產(chǎn)生，每一位患者都完成了長達三周的訓(xùn)練,，其每天都進行言語交流的訓(xùn)練,。這項新技術(shù)可以幫助患者改善自主發(fā)音的產(chǎn)生能力，可以使得中風(fēng)患者發(fā)出簡短的腳本文字，并且可以輕松告訴別人,。于此同時神經(jīng)影像技術(shù)也幫助研究者更深入地理解了“言語誘導(dǎo)”發(fā)生的機制,。
研究者Fridriksson說，前期研究揭示了言語誘導(dǎo)的訓(xùn)練可以改善布羅卡氏失語癥患者言語產(chǎn)生的能力,，這就為開發(fā)相應(yīng)的治療中風(fēng)患者失語癥的新型療法提供了幫助和希望,。（生物谷Bioon.com）
doi:10.1093/brain/aws301
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Speech entrainment enables patients with Broca’s aphasia to produce fluent speech
Julius Fridriksson1, H. Isabel Hubbard1, Sarah Grace Hudspeth1, Audrey L. Holland2, Leonardo Bonilha3, Davida Fromm4 and Chris Rorden5
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.
