Hess C W, Hunziker T, Küpfer A, Ludin H P
J Neurol. 1986 Apr;233(2):83-9. doi: 10.1007/BF00313852.
Prospective clinical and electrophysiological follow-up was performed on nine patients under thalidomide treatment in order to detect the very beginning of possible drug-induced peripheral neuropathy. For neurophysiological assessment, nerve conduction measurements of the median, peroneal and sural nerves (7 conduction parameters) and needle EMG examination of the anterior tibial muscle were performed. The results of a first control after about 3 months of treatment were compared with the starting point examination, and the patients were then classified as "affected" or "not affected" according to clinical and neurophysiological criteria. At this point, three patients showed clinical and electrophysiological, and another two only electrophysiological alterations suggesting early neuropathy. This classification did not change after further clinical and electrophysiological controls. Without starting-point values, the early detection of neuropathy would not have been possible in all patients. No single reliable neurophysiological parameter for detection of thalidomide-induced neuropathy could be found. Pharmacogenetic classification with regard to hydroxylation and acetylation phenotypes was then performed in some patients and interpreted with relation to thalidomide neurotoxicity. A possible relationship between slow acetylators and development of thalidomide-induced neuropathy was found.
对9例接受沙利度胺治疗的患者进行了前瞻性临床和电生理随访，以检测可能的药物性周围神经病变的最初迹象。为进行神经生理学评估，对正中神经、腓总神经和腓肠神经进行了神经传导测量（7个传导参数），并对胫前肌进行了针极肌电图检查。将治疗约3个月后的首次对照结果与起始检查结果进行比较，然后根据临床和神经生理学标准将患者分为“受影响”或“未受影响”。此时，3例患者出现临床和电生理改变，另外2例仅出现提示早期神经病变的电生理改变。在进一步的临床和电生理对照后，这种分类没有改变。如果没有起始值，就不可能在所有患者中早期发现神经病变。未发现单一可靠的用于检测沙利度胺所致神经病变的神经生理学参数。随后对部分患者进行了关于羟基化和乙酰化表型的药物遗传学分类，并结合沙利度胺神经毒性进行了解释。发现慢乙酰化者与沙利度胺所致神经病变的发生之间可能存在关联。
