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Brain Activation Site of Laryngeal Elevation During Swallowing: An fMRI Study
Zhiyi Zhang1,2, Ling Yan3, Xiangxin Xing1,4,5
1School of Rehabilitation Science, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Abstract:
The object of this study is to investigate dysphagia caused by reduced laryngeal elevation in patients poststroke. The central mechanism of laryngeal elevation during swallowing was explored by comparing the brain activation area before and after treatment with that of healthy subjects. The treatment group included patients diagnosed with dysphagia poststroke that showed reduced laryngeal elevation. They were treated with electrical stimulation at the motor points of the muscles related to laryngeal elevation. Functional magnetic resonance imaging (fMRI) using the blood oxygenation level-dependent (BOLD) was used to observe brain activation of the normal healthy control group and treatment group during voluntary swallowing. Independent sample t test and paired sample t test were used to analyze the differences in brain activation between and within the groups. Compared with the control group, no activation was observed in the brainstem and putamen regions of the experimental group before treatment. Statistics showed that the experimental group had a wider range of brain activation than the control group pretreatment, including the left supplementary motor area, the cingulate gyrus, the inferior frontal gyrus, the right thalamus, and the right putamen. After the electrical stimulation, the brain stem subregion, the left cerebellar lobule IV and V, and parts of the cerebral cortex were more active, while the left supplementary motor area, paracentral lobule, and occipital lobule were less active post-treatment. (1) The brainstem and putamen are the specific brain regions that control laryngeal movement. (2) The enhanced activation of the cortical-basal ganglia-thalamic circuit after stroke is a compensatory mechanism. (3) The improvement of hyoid bone elevation was related to the enhanced activation of the IV and V lobes of the cerebellar hemisphere. The over-activation of the supplementary motor area poststroke would subside once the motor function improved.
