Palakurthy P R, Iyer V, Meckler R J
Arch Intern Med. 1987 May;147(5):881-4.
One hundred two patients with recurrent, drug-refractory tachyarrhythmias were treated with amiodarone for nine +/- eight months (mean +/- SD) (range, one to 50 months). Forty-five patients exhibited some form of neurotoxic reaction that was severe enough in nine patients to require discontinuation of treatment or reduction in dosage of the drug. The most frequent neurotoxic findings were tremor (44 patients), peripheral neuropathy (ten patients), and ataxia (seven patients). Five patients developed unusual neurotoxic manifestations: brainstem dysfunction characterized by downbeat nystagmus, hemisensory loss and ataxia, severe dyskinesia, jaw tremor, and proximal myopathy. Neurophysiologic studies revealed varying degrees of predominantly demyelinating peripheral neuropathy. Neurotoxic symptoms improved after discontinuing treatment or decreasing the dosage of the drug. Age of the patient and total cumulative dose did not seem to be risk factors for development of neurotoxicity. These neurotoxic findings suggest that amiodarone-induced neurotoxic reactions are not only confined to the peripheral nervous system, but also that parts of the central nervous system (eg, basal ganglia, brain stem, or their connections) may also be involved.
102例复发性、药物难治性快速心律失常患者接受了胺碘酮治疗,疗程为9±8个月(平均±标准差)(范围为1至50个月)。45例患者出现了某种形式的神经毒性反应,其中9例严重到需要停药或减少药物剂量。最常见的神经毒性表现为震颤(44例患者)、周围神经病变(10例患者)和共济失调(7例患者)。5例患者出现了不寻常的神经毒性表现:以向下凝视性眼球震颤、偏身感觉丧失和共济失调为特征的脑干功能障碍、严重的运动障碍、下颌震颤和近端肌病。神经生理学研究显示主要为脱髓鞘性周围神经病变的不同程度。停药或减少药物剂量后神经毒性症状有所改善。患者年龄和总累积剂量似乎不是发生神经毒性的危险因素。这些神经毒性表现提示,胺碘酮所致神经毒性反应不仅局限于周围神经系统,而且中枢神经系统的某些部分(如基底神经节、脑干或它们的连接部位)也可能受累。