Nagasawa Hikaru, Wada Manabu, Kurita Keiji, Iseki Chihumi, Katagiri Tadashi, Kato Takeo
Department of Neurology, Hematology, Metabolism, Endocrinology and Diabetology (DNHMED), Yamagata University School of Medicine.
Rinsho Shinkeigaku. 2006 May;46(5):322-7.
This is a report of a 31-year-old woman with non-herpetic acute limbic encephalitis following a type-2 adenovirus infection. The patient was admitted to a hospital with high fever, severe liver dysfunction, and thrombocytopenia. Six days after admission, she became afebrile, and her liver dysfunction was normalized by conservative therapy. However, the patient started to experience generalized seizures that developed into status epileptics. The patient was then transferred to a referred hospital. Brain MR images revealed faint high-signal intensity in the bilateral limbic systems on FLAIR images. A CSF examination indicated mild pleocytosis. These findings suggested acute limbic encephalitis, which may have been mediated by an autoimmune reaction following some viral infection. Thus, steroid pulse therapy was started on the day of admission. The patient's condition, including the seizures and disturbances involving consciousness, improved gradually. The patient was discharged from the hospital in one month while still experiencing mild memory disturbances. Three months after onset of the illness, a T1-weighted MR image showed a linear high-signal intensity in the hippocampi, which indicated focal necrosis. Six months after onset, the patient's memory disturbance had been improved (her MMSE score was 28/30 points). We investigated the titers of many viruses that are known to cause liver dysfunction and found that a titer of the type-2 adenovirus was significantly elevated within three weeks. Although the anti-voltage-gated potassium channel (VGKC) antibody was not detected in the patient's serum, it seems that the autoimmune reaction after the type-2 adenovirus infection may have caused the acute limbic encephalitis.
这是一篇关于一名31岁女性的报告,该患者在感染2型腺病毒后患上非疱疹性急性边缘叶脑炎。患者因高热、严重肝功能不全和血小板减少症入院。入院六天后,她体温恢复正常,肝功能通过保守治疗恢复正常。然而,患者开始出现全身性癫痫发作,并发展为癫痫持续状态。随后患者被转至一家转诊医院。脑部磁共振成像(MR)图像在液体衰减反转恢复(FLAIR)序列上显示双侧边缘系统有模糊的高信号强度。脑脊液检查显示轻度细胞增多。这些发现提示为急性边缘叶脑炎,可能是由某种病毒感染后的自身免疫反应介导的。因此,在入院当天开始使用类固醇脉冲疗法。患者的病情,包括癫痫发作和意识障碍逐渐改善。患者在一个月后出院,但仍有轻度记忆障碍。发病三个月后,T1加权MR图像显示海马体有线性高信号强度,提示局灶性坏死。发病六个月后,患者的记忆障碍有所改善(简易精神状态检查表(MMSE)评分为28/30分)。我们检测了许多已知可导致肝功能不全的病毒的滴度,发现2型腺病毒的滴度在三周内显著升高。尽管在患者血清中未检测到抗电压门控钾通道(VGKC)抗体,但似乎2型腺病毒感染后的自身免疫反应可能导致了急性边缘叶脑炎。