Koguchi Y, Yagishita T, Sato A, Watanabe Y
Department of Neurology, Chiba Emergency Medical Center.
Rinsho Shinkeigaku. 1996 Nov;36(11):1225-8.
Epstein-Barr virus (EBV) infection is occasionally accompanied by acute neurological impairment. The pathogenesis of neurological manifestations with EBV infection consists of primary inflammations of EBV infection, and secondary immunologic reactions. However, their clinical course and prognosis are usually favorable. Here we report a patient with fulminant neurological involvement in association with EBV infection. The patient was a 44-year-old man. One morning he developed ataxic gait and speech following flu-like symptoms. He noticed double vision in the afternoon. He had disturbance of consciousness, bilateral ptosis with mydriasis, opthalmoplegia, facial diplegia, bulbar palsy, and weakness of muscles in extremities and respiratory system on the next day. He required mechanical ventilatory support for a month. His symptoms began to improve gradually two weeks after the onset. Two month later, neurological examinations disclosed severe cerebellar ataxia of the four extremities and ocular movement, cerebellar speech, and moderate weakness in his limbs. Moderate cerebellar ataxia and diminished deep tendon reflexes remained for 8-months. Although he had no physical manifestations of infectious mononucleosis, DNA of EBV was identified in the cerebrospinal fluid (CSF) by the polymerase chain reaction method. From these results, we diagnosed his condition as a cerebello brainstem encephalitis with polyradiculitis associated with EBV infection. The cell counts and protein content of CSF gradually normalized in the early stage of his illness, but CSF protein increased again, and had the peak of 275 mg/dl in about one month. In spite of normalized CSF cell counts, his neurological symptoms persisted. CT scan and MRI studies of the brain and the spinal cord were repeated, but demonstrated no significant abnormalities. Clinical course and CSF findings revealed that his fulminant neurological symptoms were most likely produced by the secondary immunologic reactions following the primary inflammations by EBV infection.
爱泼斯坦-巴尔病毒（EBV）感染偶尔会伴有急性神经功能损害。EBV感染所致神经表现的发病机制包括EBV感染的原发性炎症和继发性免疫反应。然而，其临床病程和预后通常良好。在此，我们报告一例与EBV感染相关的暴发性神经受累患者。该患者为一名44岁男性。一天早晨，他在出现类似流感症状后出现共济失调步态和言语障碍。下午他注意到复视。第二天，他出现意识障碍、双侧上睑下垂伴瞳孔散大、眼球麻痹、面瘫、延髓麻痹以及四肢和呼吸系统肌肉无力。他需要机械通气支持一个月。发病两周后他的症状开始逐渐改善。两个月后，神经检查发现四肢和眼球运动存在严重的小脑性共济失调、小脑性言语以及肢体中度无力。中度小脑性共济失调和腱反射减弱持续了8个月。尽管他没有传染性单核细胞增多症的体征，但通过聚合酶链反应法在脑脊液（CSF）中检测到了EBV DNA。根据这些结果，我们将他的病情诊断为与EBV感染相关的伴有多发性神经根炎的小脑脑干脑炎。患者发病早期脑脊液的细胞计数和蛋白含量逐渐恢复正常，但脑脊液蛋白再次升高，约一个月时达到275mg/dl的峰值。尽管脑脊液细胞计数恢复正常，但其神经症状仍持续存在。对脑和脊髓反复进行CT扫描和MRI检查，但未发现明显异常。临床病程和脑脊液检查结果表明，他的暴发性神经症状很可能是由EBV感染引发的原发性炎症后的继发性免疫反应所致。
