中华物理医学与康复杂志
中華物理醫學與康複雜誌
중화물리의학여강복잡지
CHINESE JOURNAL OF PHYSICAL MEDICINE AND REHABILITATION
2009年
12期
812-816
,共5页
魏新华%戴建平%沈慧聪%张婧%李少武%艾林%马军%江新青
魏新華%戴建平%瀋慧聰%張婧%李少武%艾林%馬軍%江新青
위신화%대건평%침혜총%장청%리소무%애림%마군%강신청
脑卒中%吞咽障碍%功能性磁共振成像%康复%神经可塑性
腦卒中%吞嚥障礙%功能性磁共振成像%康複%神經可塑性
뇌졸중%탄인장애%공능성자공진성상%강복%신경가소성
Stroke%Dysphagia%Functional magnetic resonance imaging%Rehabilitation%Neuronal plasticity
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吞咽障碍组,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吞咽功能基本康复的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3.0 T超导磁共振成像仪及回波平面成像(EPI)T_2加权成像(T_2WI)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、后激活脑容积的大小及LI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、前扣带同等.康复组中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LI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.
目的 使用功能性磁共振成像技術研究患者腦卒中後吞嚥障礙的康複機製.方法 選取13例有單側皮質或皮質下病竈的腦卒中首次閤併吞嚥障礙的患者作為吞嚥障礙組,對吞嚥障礙組患者行2~3週的吞嚥障礙綜閤康複治療;另選8例年齡匹配的健康誌願者作為對照組.分彆對2組行自主吞嚥任務功能性磁共振成像檢查.把吞嚥障礙組中經治療後吞嚥功能基本康複的7例患者設為康複組併行功能性磁共振成像複查.功能性磁共振成像數據採集採用3.0 T超導磁共振成像儀及迴波平麵成像(EPI)T_2加權成像(T_2WI)序列,統計參數圖軟件用于功能性磁共振成像數據後處理;併計算偏側性繫數(LI)=(C-I)/(C+I)(C為對側半毬激活腦體積,I為同側半毬激活腦體積);對康複組患者康複前、後激活腦容積的大小及LI值的進行配對t檢驗.結果 對照組激活腦區有雙側初級感覺運動皮質、前釦帶迴、雙側島葉等腦區.吞嚥障礙組激活腦區位于腦橋、延髓、左側小腦、左側額前區、右枕葉、左側島葉等腦區.康複組激活腦區有雙側感覺運動區、雙側額前區、雙顳上中迴、左島葉、雙側島蓋、前釦帶同等.康複組中康複前病竈側激活腦區容積小于病竈對側激活腦區容積,差異有統計學意義(P<0.01),康複後病竈側激活腦容積大于康複前病竈側激活腦容積,差異有統計學意義(P<0.01);康複後LI值大于康複前LI值,差異有統計學意義(P<0.01).結論 感覺運動區、島葉及釦帶迴等腦區激活減少或消失是導緻吞嚥障礙的原因.腦卒中後吞嚥障礙康複前由健側腦區部分代償、康複後患側吞嚥相關腦區的激活可能是吞嚥障礙康複機製之一.
목적 사용공능성자공진성상기술연구환자뇌졸중후탄인장애적강복궤제.방법 선취13례유단측피질혹피질하병조적뇌졸중수차합병탄인장애적환자작위탄인장애조,대탄인장애조환자행2~3주적탄인장애종합강복치료;령선8례년령필배적건강지원자작위대조조.분별대2조행자주탄인임무공능성자공진성상검사.파탄인장애조중경치료후탄인공능기본강복적7례환자설위강복조병행공능성자공진성상복사.공능성자공진성상수거채집채용3.0 T초도자공진성상의급회파평면성상(EPI)T_2가권성상(T_2WI)서렬,통계삼수도연건용우공능성자공진성상수거후처리;병계산편측성계수(LI)=(C-I)/(C+I)(C위대측반구격활뇌체적,I위동측반구격활뇌체적);대강복조환자강복전、후격활뇌용적적대소급LI치적진행배대t검험.결과 대조조격활뇌구유쌍측초급감각운동피질、전구대회、쌍측도협등뇌구.탄인장애조격활뇌구위우뇌교、연수、좌측소뇌、좌측액전구、우침협、좌측도협등뇌구.강복조격활뇌구유쌍측감각운동구、쌍측액전구、쌍섭상중회、좌도협、쌍측도개、전구대동등.강복조중강복전병조측격활뇌구용적소우병조대측격활뇌구용적,차이유통계학의의(P<0.01),강복후병조측격활뇌용적대우강복전병조측격활뇌용적,차이유통계학의의(P<0.01);강복후LI치대우강복전LI치,차이유통계학의의(P<0.01).결론 감각운동구、도협급구대회등뇌구격활감소혹소실시도치탄인장애적원인.뇌졸중후탄인장애강복전유건측뇌구부분대상、강복후환측탄인상관뇌구적격활가능시탄인장애강복궤제지일.
Objective To study the recovery mechanism of dysphagic patients after stroke using functional magnetic resonanee imaging(fMRI). Methods Thirteen patients with dysphagia caused by unilateral cortical or subcortical lesions were recruited into a dysphagia group,and eight age-matched healthy volunteers were recruited as controls.Both grouDs performed experimental volitional swallowing tasks during fMRI studies.All patients of the dys-phagia 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(EPI)T_2 WI 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-1)/(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 o-pereulum and anterior cingulated gyrus in the recovered patients.The total activated volume before recovery in the ip-silesional hemisDhere 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 significant-ly larger than those at the initial examination.Conclusions Decreased activation in the sensorimotor cortex,the in-sular lobe and the cingulate gyms 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.