Institute for Biomagnetism and Biosignalanalysis, University of Muenster, Malmedyweg 15, 48149 Muenster, Germany.
Brain. 2013 Mar;136(Pt 3):726-38. doi: 10.1093/brain/awt004. Epub 2013 Feb 14.
Dysphagia is a relevant symptom in Parkinson's disease, whose pathophysiology is poorly understood. It is mainly attributed to degeneration of brainstem nuclei. However, alterations in the cortical contribution to deglutition control in the course of Parkinson's disease have not been investigated. Here, we sought to determine the patterns of cortical swallowing processing in patients with Parkinson's disease with and without dysphagia. Swallowing function in patients was objectively assessed with fiberoptic endoscopic evaluation. Swallow-related cortical activation was measured using whole-head magnetoencephalography in 10 dysphagic and 10 non-dysphagic patients with Parkinson's disease and a healthy control group during self-paced swallowing. Data were analysed applying synthetic aperture magnetometry, and group analyses were done using a permutation test. Compared with healthy subjects, a strong decrease of cortical swallowing activation was found in all patients. It was most prominent in participants with manifest dysphagia. Non-dysphagic patients with Parkinson's disease showed a pronounced shift of peak activation towards lateral parts of the premotor, motor and inferolateral parietal cortex with reduced activation of the supplementary motor area. This pattern was not found in dysphagic patients with Parkinson's disease. We conclude that in Parkinson's disease, not only brainstem and basal ganglia circuits, but also cortical areas modulate swallowing function in a clinically relevant way. Our results point towards adaptive cerebral changes in swallowing to compensate for deficient motor pathways. Recruitment of better preserved parallel motor loops driven by sensory afferent input seems to maintain swallowing function until progressing neurodegeneration exceeds beyond the means of this adaptive strategy, resulting in manifestation of dysphagia.
吞咽困难是帕金森病的一个相关症状，但其病理生理学尚未被充分理解。它主要归因于脑干核的退化。然而，在帕金森病的过程中，皮质对口咽控制的贡献的改变尚未被研究。在这里，我们试图确定有和没有吞咽困难的帕金森病患者的皮质吞咽处理模式。使用纤维内镜评估对患者的吞咽功能进行客观评估。使用全头磁强计在 10 名有吞咽困难的帕金森病患者和 10 名无吞咽困难的帕金森病患者以及健康对照组中测量与吞咽相关的皮质激活，在自我控制的吞咽过程中进行测量。使用合成孔径磁强计对数据进行分析，并使用置换检验进行组分析。与健康受试者相比，所有患者的皮质吞咽激活均明显下降。在有明显吞咽困难的参与者中最为明显。帕金森病无吞咽困难的患者表现出明显的向运动前、运动和下外侧顶叶皮质的外侧部分的激活峰值转移，而辅助运动区的激活减少。在帕金森病伴吞咽困难的患者中未发现这种模式。我们得出结论，在帕金森病中，不仅脑干和基底节回路，而且皮质区域也以临床相关的方式调节吞咽功能。我们的结果表明，在吞咽过程中，适应性的大脑变化可以补偿运动通路的缺陷。由感觉传入输入驱动的更好保存的平行运动回路的募集似乎可以维持吞咽功能，直到进展性神经退行性变超出这种适应性策略的能力，导致吞咽困难的表现。
