脑卒中后吞咽障碍康复机制的功能性磁共振成像研究

Mechanism of recovery of dysphagic patients caused by stroke： A fMRI study

目的 使用功能性磁共振成像技术研究患者脑卒中后吞咽障碍的康复机制。方法选取13例有单侧皮质或皮质下病灶的脑卒中首次合并吞咽障碍的患者作为乔咽障碍组，对吞咽障碍组患者行2～3周的吞咽障碍综合康复治疗；另选8例年龄匹配的健康志愿者作为对照组。分别对2组行自主吞咽任务功能性磁共振成像检查。把吞咽障碍组中经治疗后乔咽功能基本康复的7例患者设为康复组并行功能性磁共振成像复查。功能性磁共振成像数据采集采用3．0T超导磁共振成像仪及回波平面成像（EPI）T，加权成像（T2WI）序列，统计参数图软件用于功能性磁共振成像数据后处理；并计算偏侧性系数（LI）=（C—I）／（C＋I）（C为对侧半球激活脑体积，I为同侧半球激活脑体积）；对康复组患者康复前、后激活脯容积的大小及L1值的进行配对t检验。结果对照组激活脑区有双侧初级感觉运动皮质、前扣带回、双侧岛叶等脑区。吞咽障碍组激活脑区位于脑桥、延髓、左侧小脑、左侧额前区、右枕叶、左侧岛叶等脑区。康复组激活脑区有双侧感觉运动区、双侧额前区、双颞上中回、左岛叶、双侧岛盖、前扣带回等。康复组巾康复前病灶侧激活脑区容积小于病灶对侧激活脑区容积，差异有统计学意义（P〈0．01），康复后病灶侧激活脑容积大于康复前病灶侧激活脑容积，差异有统计学意义（P〈0．01）；康复后L1值大于康复前LI值，差异有统计学意义（P〈0．01）。结论 感觉运动区、岛叶及扣带回等脑区激活减少或消失是导致吞咽障碍的原因。脑卒中后吞咽障碍康复前由健侧脑区部分代偿、康复后患侧吞咽相关脑区的激活可能是吞咽障碍康复机制之一。

magnetic resonance Objective To study the recovery mechanism of dysphagic patients after stroke using functional imaging （fMRI）. Methods Thirteen patients with dysphagia caused by unilateral cortical or subeortical lesions were recruited into a dysphagia group, and eight age-matched healthy volunteers were recruited as controls. Both groups performed experimental volitional swallowing tasks during fMRI studies. All patients of the dysphagia group received rehabilitation treatment targeting dysphagia. Of the 13 dysphagia patients, 7 reached almost complete recovery and were identified as recovered in follow-up fMRI studies. A 3.0 T MR scanner and echo planar imaging （EP1） T2WI sequence were employed to obtain the fMRI data. SPM2 software was used for post-processing of the fMRI data and displaying activated brain maps. Lateral index （LI） was calculated as LI = （ C - I）/ （ C ＋ I）. Paired t tests were used to compare activated brain volume before and after complete recovery. Results Consistent activation of the bilateral primary sensorimotor cortex, anterior cingulated gyrus and the bilateral insular cortex were observed in the control group. Activation of the pons, medulla, left cerebellum, left prefrontal area, right occipital area and the left insular cortex were observed in the dysphagia group. Activation was observed in the bilateral primary sensorimotor cortex, bilateral prefrontal area, bilateral superior temporal gyrus, left insular cortex, bilateral frontal operculum and anterior cingulated gyrus in the recovered patients. The total activated volume before recovery in the ipsilesional hemisphere was significantly less compared with the contralesional hemisphere in the dysphagia group. In the recovered patients, both the activated brain volume of the ipsilesional hemisphere and value of LI were significantly larger than those at the initial examination. Conclusions Decreased activation in the sensorimotor cortex, the insular lobe and the cingulate gyrus might be causes, of dysphagia. Compensation by the contralesional hemisphere in the early stages and then the restoration of the ipsilesional hemisphere after recovery may be mechanisms of dysphagia recovery in stroke patients.