Schied H W, Bartels M
Pharmacopsychiatria. 1983 Mar;16(2):64-7. doi: 10.1055/s-2007-1017451.
Transitory ataxias have repeatedly been observed and reported in connection with antidepressant medication. However, it is remarkable that exact descriptions of this particular form of ataxia are rarely included. Also, hypotheses concerning the etiology and pathophysiology of these disorders are generally lacking. They are usually given the imprecise designation of "extrapyramidal" ataxias. Two cases are presented here in which therapy-resistant endogenous depressions were treated with maprotiline/dibenzepine and maprotiline/clomipramine, respectively. In both cases, marked neurological side effects in the form of cerebellar ataxia developed. The symptoms, which occurred despite usual dosage, remitted after maprotiline treatment was discontinued for one patient and after dose reduction of both drugs for the other. The atactical and dysmetric symptoms described here are thought to result from a reversible intoxication of mainly cerebellar structures. In an attempt to explain the genesis of these ataxias, a neurophysiological and a neuropharmacological hypothesis are considered and predisposing factors as well as therapeutic consequences are discussed.
与抗抑郁药物相关的短暂性共济失调已被反复观察和报道。然而，值得注意的是，这种特殊形式的共济失调的确切描述很少被纳入其中。此外，关于这些疾病的病因和病理生理学的假设普遍缺乏。它们通常被不精确地称为“锥体外系”共济失调。本文介绍了两例病例，分别用马普替林/二苯并氮䓬和马普替林/氯米帕明治疗难治性内源性抑郁症。在这两例病例中，均出现了以小脑性共济失调为表现的明显神经副作用。尽管使用了常规剂量，症状仍出现，其中一例患者停用马普替林治疗后症状缓解，另一例患者两种药物剂量减少后症状缓解。这里描述的共济失调和辨距不良症状被认为是主要小脑结构可逆性中毒的结果。为了解释这些共济失调的发生机制，考虑了一种神经生理学和一种神经药理学假设，并讨论了诱发因素以及治疗后果。
