Peiffer J
Arch Psychiatr Nervenkr (1970). 1981;231(1):41-60. doi: 10.1007/BF00342829.
A female patient, who died at the age of 61 and had suffered from several manic-depressive psychoses for more than 30 years, developed three phases of intoxication under lithium therapy. There was a 15-year history of electro- and Pentetrazol-induced convulsive therapy prior to lithium medication; neuroleptics were still administered during lithium therapy. The last lithium intoxication, 3 years prior to death was during a low-dosage therapy with normal lithium levels followed by severe lasting impairment: akinesia, rigidity, dysarthria, ataxia, and an organic alteration in character. For the first time, neuropathological findings could be established in such a case: extensive damage to granule and Purkinje cells in the cerebellum; gliosis in the dentate nucleus, the inferior olives, and the nucleus ruber; cytoplasmic inclusions in various nerve cells of the cranial nerve nuclei; cytoplasmic vacuoles, especially in the cells of the supra-optic nucleus. Surprisingly little damage could be found in the substantia nigra and in the neostriatum. The clinical course as well as the pattern and intensity of the brain damage oppose an interpretation as a consequence of preceding convulsive shock therapy.
一名61岁女性患者,患躁狂抑郁症30多年,在锂盐治疗期间出现了三个阶段的中毒反应。在开始锂盐治疗前,有15年电休克和戊四氮诱导惊厥治疗史;在锂盐治疗期间仍使用抗精神病药物。死前3年的最后一次锂中毒发生在低剂量治疗且血锂水平正常时,随后出现严重的持续性损害:运动不能、强直、构音障碍、共济失调以及性格器质性改变。首次在这种病例中确定了神经病理学发现:小脑颗粒细胞和浦肯野细胞广泛受损;齿状核、下橄榄核和红核出现胶质增生;脑神经核的各种神经细胞中有细胞质包涵体;细胞质空泡,尤其是视上核细胞中。黑质和新纹状体的损伤出人意料地少。临床病程以及脑损伤的类型和严重程度与先前惊厥休克治疗的结果不符。