Cortical processing of swallowing in ALS patients with progressive dysphagia--a magnetoencephalographic study.
Cortical processing of swallowing in ALS patients with progressive dysphagia--a magnetoencephalographic study.
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DOI：
10.1371/journal.pone.0019987
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发表时间：
2011
期刊：
影响因子：
3.7
通讯作者：
Dziewas R
中科院分区：
文献类型：
--
作者：
Teismann IK;Warnecke T;Suntrup S;Steinsträter O;Kronenberg L;Ringelstein EB;Dengler R;Petri S;Pantev C;Dziewas R
肌萎缩性侧索硬化症（ALS）是一种罕见的疾病，引起上下运动神经元变性。累及球运动神经元常导致快速进行性吞咽困难。虽然大脑皮层代偿在中风患者中已被证实，但在ALS患者中尚未发现。在本研究中，我们研究了两组患有中度或重度吞咽困难的ALS患者在吞咽过程中的皮质激活。采用自主节奏吞咽模式，对14例散发性ALS患者采用全头部MEG。采用时频分析和合成孔径磁强计（SAM）对数据进行分析。使用置换检验对个体SAM数据进行分组分析。我们发现，与健康对照相比，ALS患者的皮质吞咽相关激活减少。此外，还观察到与疾病相关的半球偏侧移位。健康受试者表现为双侧皮层激活，而ALS患者的右侧感觉运动皮层主要参与。这两种效果在严重吞咽困难患者组中更为明显。我们的研究结果表明，初级运动区域的双侧上运动神经元的退化也会损害进一步调整的运动区域，从而导致“吞咽相关”皮层激活的强烈减少。虽然两个半球都受到退化的影响，但右半球的激活程度相对较强。本研究中观察到的意志吞咽的右半球偏侧可能是吞咽困难的ALS患者大脑皮层可塑性的唯一标志。它可能表明补偿机制在右半球，这是已知的主要协调咽部吞咽。这些结果为我们对ALS患者吞咽困难的病理生理学的理解增加了新的方面。观察到的代偿机制可能与未来的吞咽治疗研究有关。
Amyotrophic lateral sclerosis (ALS) is a rare disease causing degeneration of the upper and lower motor neuron. Involvement of the bulbar motor neurons often results in fast progressive dysphagia. While cortical compensation of dysphagia has been previously shown in stroke patients, this topic has not been addressed in patients suffering from ALS. In the present study, we investigated cortical activation during deglutition in two groups of ALS patients with either moderate or severe dysphagia. Whole-head MEG was employed on fourteen patients with sporadic ALS using a self-paced swallowing paradigm. Data were analyzed by means of time-frequency analysis and synthetic aperture magnetometry (SAM). Group analysis of individual SAM data was performed using a permutation test. We found a reduction of cortical swallowing related activation in ALS patients compared to healthy controls. Additionally a disease-related shift of hemispheric lateralization was observed. While healthy subjects showed bilateral cortical activation, the right sensorimotor cortex was predominantly involved in ALS patients. Both effects were even stronger in the group of patients with severe dysphagia. Our results suggest that bilateral degeneration of the upper motor neuron in the primary motor areas also impairs further adjusted motor areas, which leads to a strong reduction of ‘swallowing related’ cortical activation. While both hemispheres are affected by the degeneration a relatively stronger activation is seen in the right hemisphere. This right hemispheric lateralization of volitional swallowing observed in this study may be the only sign of cortical plasticity in dysphagic ALS patients. It may demonstrate compensational mechanisms in the right hemisphere which is known to predominantly coordinate the pharyngeal phase of deglutition. These results add new aspects to our understanding of the pathophysiology of dysphagia in ALS patients and beyond. The compensational mechanisms observed could be relevant for future research in swallowing therapies.
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