Reduced tongue force and functional swallowing changes in a rat model of post stroke dysphagia

Reduced tongue force and functional swallowing changes in a rat model of post stroke dysphagia
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DOI:
10.1016/j.brainres.2019.04.023
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发表时间:
2019-08-15
期刊:
影响因子:
2.9
通讯作者:
Connor, Nadine P.
Connor, Nadine P.
中科院分区:
医学3区
文献类型:
--
作者:
Cullins, Miranda J.;Connor, Nadine P.

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目的:吞咽困难是中风后常见的问题,通常与舌头无力有关。然而,中风后舌肌无力的生理机制和最佳治疗方法尚未建立。为了进一步了解脑卒中后吞咽困难的生理机制,我们试图验证单侧短暂性大脑中动脉闭塞(MCAO)大鼠缺血性脑卒中模型作为脑卒中后吞咽困难的平移模型。我们的目标是建立临床相关措施和慢性功能缺陷;增加研究结果转化为临床应用的可能性的标准。我们假设MCAO会导致舌头无力和吞咽功能改变。方法:收集8周龄雄性Sprague-Dawley大鼠在接受左侧MCAO (N = 10)或假手术(N = 10)之前的最大自愿舌力和视频透视吞咽研究。术后1周和8周重新评估舌力和VFSS。结果:MCAO组在第1周和第8周时最大自主舌力、给药面积和给药速度显著降低。结论:临床相关的吞咽和舌力变化支持MCAO大鼠模型作为脑卒中后吞咽困难的翻译模型。该模型将允许未来的研究,以提高我们对这些功能变化的生理学的理解,以及治疗干预对生理目标和功能的影响。
Purpose: Dysphagia is a common problem after stroke that is often associated with tongue weakness. However, the physiological mechanisms of post-stroke tongue muscle weakness and optimal treatments have not been established. To advance understanding of physiological mechanisms of post stroke dysphagia, we sought to validate the unilateral transient middle cerebral artery occlusion (MCAO) rat model of ischemic stroke as a translational model of post stroke dysphagia. Our goal was to establish clinically relevant measures and chronicity of functional deficits; criteria that increase the likelihood that findings will translate to the clinic. We hypothesized that MCAO would cause tongue weakness and functional swallowing changes.Methods: Maximum voluntary tongue forces and videofluoroscopic swallowing studies were collected in 8-week old male Sprague-Dawley rats prior to receiving either a left MCAO (N = 10) or sham (N = 10) surgery. Tongue forces and VFSS were reassessed at 1 and 8 weeks post-surgery.Results: Maximum voluntary tongue force, bolus area, and bolus speed were significantly reduced in the MCAO group at the 1 and 8-week timepoints.Conclusion: Clinically relevant changes to swallowing and tongue force support the use of the MCAO rat model as a translational model of post stroke dysphagia. This model will allow for future studies to improve our understanding of the physiology contributing to these functional changes as well as the impact of therapeutic interventions on physiological targets and function.