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口吃者的神经异常和重组:一项短期干预研究。

Neural anomaly and reorganization in speakers who stutter: a short-term intervention study.

机构信息

State Key Laboratory of Cognitive Neuroscience and Learning, Beijing Normal University, Beijing, PR China.

出版信息

Neurology. 2012 Aug 14;79(7):625-32. doi: 10.1212/WNL.0b013e31826356d2. Epub 2012 Aug 8.

Abstract

OBJECTIVES

The aim of the current study was to differentiate between neural activity that represents neural anomalies that are responsible for persistent developmental stuttering (PDS) from the activity that is a result of compensating for stuttering. This was done by investigating alterations to the intrinsic functional architecture of speech-language processes of patients with PDS before and after a short-term intervention.

METHODS

The resting-state functional connectivity (RSFC) and cortical thickness were examined before and after the intervention. The structural data were used to validate the functional results. Fifteen stuttering patients who received intervention (PDS+), 13 stuttering patients who did not receive intervention (PDS-), and 13 fluent controls participated.

RESULTS

Before the intervention, both groups of PDS patients showed significant RSFC and cortical thickness reductions in the left pars-opercularis (PO) and RSFC increases in the cerebellum, as compared to fluent controls. The intervention was effective in reducing stuttering in PDS+ patients and lowering their RSFC in the cerebellum to the level of fluent controls. The intervention effect was specific to the PDS+ group (it was not evident in the PDS- group). The intervention did not change RSFC and cortical thickness in the left PO, which remained at its preintervention level.

CONCLUSIONS

The results suggest that the left PO is a locus where the intrinsic functional architecture of speech-language processes is altered in PDS patients, suggesting an etiologic role of this region in PDS. The cerebellum showed intervention-induced neural reorganization, suggesting a compensatory response when stuttering occurs.

摘要

目的

本研究旨在区分导致持续性发展性口吃(PDS)的神经活动和口吃补偿的神经活动。通过研究 PDS 患者在短期干预前后言语语言过程固有功能结构的变化来实现这一点。

方法

在干预前后检查静息状态功能连接(RSFC)和皮质厚度。结构数据用于验证功能结果。15 名接受干预的口吃患者(PDS+)、13 名未接受干预的口吃患者(PDS-)和 13 名流利对照组参与了研究。

结果

干预前,与流利对照组相比,两组 PDS 患者的左侧额下回(PO)均显示出显著的 RSFC 和皮质厚度降低,小脑的 RSFC 增加。干预在 PDS+患者中有效减少了口吃,并将其小脑的 RSFC 降低到流利对照组的水平。干预效果是 PDS+组特有的(在 PDS-组中不明显)。干预没有改变左侧 PO 的 RSFC 和皮质厚度,仍保持在干预前的水平。

结论

结果表明,左侧 PO 是 PDS 患者言语语言过程固有功能结构改变的部位,提示该区域在 PDS 中起病因作用。小脑显示出干预诱导的神经重组,表明口吃发生时的代偿反应。

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