中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2010年
4期
374-378
,共5页
陈颉%司志超%赵光宇%王光彬%栾立明%丁峰%武乐斌%庞琦
陳頡%司誌超%趙光宇%王光彬%欒立明%丁峰%武樂斌%龐琦
진힐%사지초%조광우%왕광빈%란립명%정봉%무악빈%방기
颅内压增高%脑静脉系统%脑桥静脉%磁共振静脉血管成像
顱內壓增高%腦靜脈繫統%腦橋靜脈%磁共振靜脈血管成像
로내압증고%뇌정맥계통%뇌교정맥%자공진정맥혈관성상
Increased intracranial pressure%Cerebral venous system%Brain bridging vein%MR venography
目的 对比观察颅内压增高与正常压力状态下脑静脉系统流出端的影像学特征,描述该段血管汇入静脉窦前的狭窄形成,结合前期实验结果探讨脑静脉系统参与颅内压调节机制中该血管狭窄节段可能的生物学意义及临床应用价值. 方法 选取40例颅内占位性病变(非血管性疾病)致颅内压增高患者为研究对象,10例正常志愿者作为对照组,磁共振静脉血管成像技术扫描成像,获得脑桥静脉及脑内静脉窦原始影像,以最大强度投影进行图像后处理,记录脑桥静脉汇入静脉窦前即两者交界处的影像学特征.并测量不同压力状态下脑桥静脉的直径.结果 颅内高压患者的脑桥静脉直径大于对照组,并且大部分颅内压增高患者(32/40)可出现影像学上脑静脉流出端磁共振信号的减弱甚至消失,形成影像学上的明显狭窄,而正常志愿者中仅有1例出现类似的信号减弱.结论 脑桥静脉作为脑静脉系统的最后通路,在颅内压增高时形成的狭窄结构提示其可能参与脑静脉系统自身体积变化的被动调节,进而对颅内压的调节发挥重要的作用.压力增高时脑桥静脉直径增加也从另外一方面说明该狭窄结构限制了静脉血液向颅外的顺畅引流,导致静脉血液的淤积并进一步增加了颅内压力.
目的 對比觀察顱內壓增高與正常壓力狀態下腦靜脈繫統流齣耑的影像學特徵,描述該段血管彙入靜脈竇前的狹窄形成,結閤前期實驗結果探討腦靜脈繫統參與顱內壓調節機製中該血管狹窄節段可能的生物學意義及臨床應用價值. 方法 選取40例顱內佔位性病變(非血管性疾病)緻顱內壓增高患者為研究對象,10例正常誌願者作為對照組,磁共振靜脈血管成像技術掃描成像,穫得腦橋靜脈及腦內靜脈竇原始影像,以最大彊度投影進行圖像後處理,記錄腦橋靜脈彙入靜脈竇前即兩者交界處的影像學特徵.併測量不同壓力狀態下腦橋靜脈的直徑.結果 顱內高壓患者的腦橋靜脈直徑大于對照組,併且大部分顱內壓增高患者(32/40)可齣現影像學上腦靜脈流齣耑磁共振信號的減弱甚至消失,形成影像學上的明顯狹窄,而正常誌願者中僅有1例齣現類似的信號減弱.結論 腦橋靜脈作為腦靜脈繫統的最後通路,在顱內壓增高時形成的狹窄結構提示其可能參與腦靜脈繫統自身體積變化的被動調節,進而對顱內壓的調節髮揮重要的作用.壓力增高時腦橋靜脈直徑增加也從另外一方麵說明該狹窄結構限製瞭靜脈血液嚮顱外的順暢引流,導緻靜脈血液的淤積併進一步增加瞭顱內壓力.
목적 대비관찰로내압증고여정상압력상태하뇌정맥계통류출단적영상학특정,묘술해단혈관회입정맥두전적협착형성,결합전기실험결과탐토뇌정맥계통삼여로내압조절궤제중해혈관협착절단가능적생물학의의급림상응용개치. 방법 선취40례로내점위성병변(비혈관성질병)치로내압증고환자위연구대상,10례정상지원자작위대조조,자공진정맥혈관성상기술소묘성상,획득뇌교정맥급뇌내정맥두원시영상,이최대강도투영진행도상후처리,기록뇌교정맥회입정맥두전즉량자교계처적영상학특정.병측량불동압력상태하뇌교정맥적직경.결과 로내고압환자적뇌교정맥직경대우대조조,병차대부분로내압증고환자(32/40)가출현영상학상뇌정맥류출단자공진신호적감약심지소실,형성영상학상적명현협착,이정상지원자중부유1례출현유사적신호감약.결론 뇌교정맥작위뇌정맥계통적최후통로,재로내압증고시형성적협착결구제시기가능삼여뇌정맥계통자신체적변화적피동조절,진이대로내압적조절발휘중요적작용.압력증고시뇌교정맥직경증가야종령외일방면설명해협착결구한제료정맥혈액향로외적순창인류,도치정맥혈액적어적병진일보증가료로내압력.
Objective To measure and compare the imaging (MRI) features of outflow segment of cerebral venous system under increased and normal intracmnial pressure (ICP) and describe the stenosis formed before the venous sinus to explore the possible biological significances and clinical values of cerebral venous system in the regulating of angiostenosis. Methods Forty patients that presented both increased ICP symptoms and more or less hydrocephalus were selected as experimental group and 10 normal volunteers were selected as control group. Both the 2 groups were underwent 2D-TOF MRI with the following parameters: repetition time/echo time, 50/4.9 milliseconds; flip angle, 45°;field of view, 250 min×250 mm; matrix, 256×256 pixels; section thickness, 1.5 mm. The original images and data of the cerebral bridging veins and cerebral venous were recorded, and then, sinus Syngo fast view imaging system was used to process and analyze them. The diameter of cerebral bridging veins under different pressures was measured. Results The diameter of cerebral bridging veins in the experimental group was longer than that in the control group. A short and narrow length in MRI was obviously shown in most increased ICP patients resulting from signal weakness even disappearance at the outflow segment of cerebral venous system, while only 1 volunteer was showed the existence of signal weakness of similar imaging. Conclusion Cerebral bridging veins, the last passageway of the cerebral venous system, can passively influence the intraeranial pressure environment to regulate the level of ICP.The increased length of diameter of cerebral bridging veins under high pressure indicates that stenosis can induce hematomain the vein by limiting the drainage of venous blood.