Terzano M G, Montanari E, Calzetti S, Mancia D, Lechi A
Arch Neurol. 1983 Sep;40(9):555-9. doi: 10.1001/archneur.1983.04050080055010.
In recent years, Creutzfeldt-Jakob disease (CJD) has been supposed to be of viral origin, and amantadine hydrochloride has been suggested as therapy because of its proved antiviral action. We studied nine patients with CJD (confirmed at autopsy in seven). Four were treated with amantadine hydrochloride, in dosages ranging from 3.5 to 15 mg/kg/day for an average period of 32 days. The clinical evolution of their disease was compared with that in five patients receiving only supportive maintenance therapy. The length of survival from the onset of clinical care did not differ significantly between the two groups. Nevertheless, a transient improvement in wakefulness and mentation was observed in three patients treated with amantadine, and EEG changes were observed in two, consisting above all of a reduction in the slow-wave activity and the periodic discharges (PDs). Amantadine administered intravenously did not induce any short-term changes in the PDs or the cyclic alternating pattern.
近年来,克雅氏病(CJD)被认为起源于病毒,由于盐酸金刚烷胺已被证实具有抗病毒作用,因此有人建议将其作为治疗药物。我们研究了9例克雅氏病患者(其中7例经尸检确诊)。4例患者接受了盐酸金刚烷胺治疗,剂量为3.5至15毫克/千克/天,平均治疗期为32天。将他们的疾病临床进展与另外5例仅接受支持性维持治疗的患者进行了比较。两组患者从临床护理开始后的存活时间没有显著差异。然而,在接受金刚烷胺治疗的3例患者中观察到清醒和精神状态有短暂改善,2例患者出现了脑电图变化,主要表现为慢波活动和周期性放电(PDs)减少。静脉注射金刚烷胺并未引起PDs或周期性交替模式的任何短期变化。