Suga T, Goto H, Yoshioka K, Hosoya T
Department of Neurosurgery, Kamaishi Municipal Hospital.
No Shinkei Geka. 1996 Nov;24(11):1051-4.
A case of Iotrolan encephalopathy is reported. A 66-year-old woman, suffering from subarachnoid hemorrhage, was admitted to our department on January 17th, 1995. After an operation for aneurysmal clipping and ventriculo-peritoneal shunt, she was discharged with no neurological deficiency. CT scan revealed ventricular enlargement and slight periventricular lucency. She was re-admitted on January 4th, 1996. She was suffering from nausea, vomiting, right hemiparesis, right hemi-hypesthesia and disturbance of consciousness. CT scan demonstrated right thalamic bleeding and bilateral ventricular hemorrhage. Further ventricular enlargement was also revealed. With medical treatment, her symptoms were relieved gradually. But disorientation and memory disturbance continued. Shuntography with Iotrolan was performed on February 2nd, 1996. The ventriculo-peritoneal shunt was demonstrated to be occluded on the abdominal side. The volume of Iotrolan used was about 8cc. She became very restless on the night of the examination. Her temperature was up to 38. CT on February 4th demonstrated brain penetration of the Iotrolan. Revision of ventriculo-peritoneal shunt, administration of steroids and hydration was performed. CSF findings demonstrated no abnormalities. Her symptoms were relieved gradually. Iotrolan is a non-ionic contrast media of dimer type, composed of C37 H48 I6 N6 O18. Its distinctive features are low distributing coefficient and high affinity with water. Contrasting several reports of Metrizamide encephalopathy, only 2 cases of Iotrolan encephalopathy were reported. Iotrolan is reported to be much safer than Metrizamide. We were able to find brain penetration by Iotrolan. It is expected to be a characteristic radiological finding of encephalopathy induced by contrast media. The mechanism of Iotrolan encephalopathy is obscure. Several theories concerning Metrizamide encephalopathy are proposed. These are (1) inhibition of hexokinase, (2) inhibition of acethylcholinesterase, (3) immunological mechanism and (4) vascular disturbance. Iotrolan has no 2-deoxy-glucose structure. The inhibition theory of hexokinase is least expected. Related matters are circulatory disturbance of liquor, dehydration, excessive contrast media, advanced age, diabetes mellitus, hypertension, epileptic patients and patients taking phenothiazines. Prompt therapy is important. Removal of contrast media, hydration and administration of steroids should be performed as early as possible.
报告了一例碘曲仑脑病病例。一名66岁女性，患有蛛网膜下腔出血，于1995年1月17日入住我科。在进行动脉瘤夹闭术和脑室 - 腹腔分流术后，她出院时无神经功能缺损。CT扫描显示脑室扩大和脑室周围轻度透亮。她于1996年1月4日再次入院。她出现恶心、呕吐、右侧偏瘫、右侧半身感觉减退和意识障碍。CT扫描显示右侧丘脑出血和双侧脑室出血。还发现脑室进一步扩大。经药物治疗，她的症状逐渐缓解。但定向障碍和记忆障碍仍持续存在。1996年2月2日进行了碘曲仑脑室造影。结果显示脑室 - 腹腔分流在腹腔侧堵塞。所用碘曲仑的量约为8cc。检查当晚她变得非常烦躁不安。体温升至38度。2月4日的CT显示碘曲仑进入脑组织。进行了脑室 - 腹腔分流术修复、给予类固醇和补液治疗。脑脊液检查结果无异常。她的症状逐渐缓解。碘曲仑是一种二聚体型非离子型造影剂，由C37 H48 I6 N6 O18组成。其显著特点是分布系数低且与水的亲和力高。与关于甲泛葡胺脑病的多篇报道相比，仅报告了2例碘曲仑脑病病例。据报道碘曲仑比甲泛葡胺安全得多。我们能够发现碘曲仑进入脑组织。这有望成为造影剂诱发脑病的特征性影像学表现。碘曲仑脑病的机制尚不清楚。提出了几种关于甲泛葡胺脑病的理论。这些理论包括：（1）己糖激酶抑制；（2）乙酰胆碱酯酶抑制；（3）免疫机制；（4）血管紊乱。碘曲仑没有2 - 脱氧 - 葡萄糖结构。己糖激酶抑制理论最不可能。相关因素包括脑脊液循环障碍、脱水、造影剂过量、高龄、糖尿病、高血压、癫痫患者以及服用吩噻嗪类药物的患者。及时治疗很重要。应尽早清除造影剂、补液并给予类固醇治疗。
