Scheller C, Strauss C, Fahlbusch R, Romstöck J
Neurochirurgische Klinik der Universität Erlangen-Nürnberg, Germany.
Zentralbl Neurochir. 2004;65(3):103-7. doi: 10.1055/s-2004-816268.
Delayed facial nerve paresis is a well known clinical phenomenon following acoustic neuroma surgery, typically occurring early during the postoperative course. The clinical course of the delayed facial nerve paresis and intraoperative electromyographic (EMG) signals were evaluated in a subgroup of patients who underwent vasoactive treatment for preservation of hearing and developed secondary deterioration after termination of treatment.
Between 1990 and 2001 seven patients were identified who received vasoactive treatment for preservation of hearing and developed a delayed facial nerve paresis after termination of medication. Intraoperative facial nerve EMG activity was analyzed in six patients.
All patients developed a delayed facial nerve paresis between 2-5 days following termination of a 10 day treatment consisting of HES and nimodipine. Medication was re-initiated and the facial nerve paresis improved in all patients. In two patients intraoperative EMG signals revealed "A-trains" waveform patterns, which are highly suggestive for an immediate postoperative facial nerve paresis, whereas in four patients no pathognomonic EMG patterns could be recorded.
The delayed onset of a facial paresis following termination of vasoactive treatment points to a disturbed microcirculation of the nerve as the main pathophysiological feature. Two groups could be identified on the basis of intraoperative EMG activity. In one group with presence of "A-trains" medication apparently masked the onset of an immediate postoperative facial nerve deficit. Four patients without "A-trains" did not develop a typical delayed facial nerve paresis during vasoactive treatment, but thereafter. The time lag between termination of treatment and onset of a delayed palsy points to a protective effect due to improved microcirculation.
迟发性面神经麻痹是听神经瘤手术后一种众所周知的临床现象，通常发生在术后早期。在一组接受血管活性药物治疗以保留听力并在治疗终止后出现继发性听力减退的患者亚组中，对迟发性面神经麻痹的临床病程及术中肌电图（EMG）信号进行了评估。
在1990年至2001年期间，确定了7例接受血管活性药物治疗以保留听力并在停药后发生迟发性面神经麻痹的患者。对其中6例患者的术中面神经EMG活动进行了分析。
所有患者在接受由羟乙基淀粉（HES）和尼莫地平组成的10天治疗停药后的2至5天内均出现迟发性面神经麻痹。重新开始用药后，所有患者的面神经麻痹均有所改善。2例患者术中EMG信号显示“A波群”波形模式，这强烈提示术后立即出现面神经麻痹，而4例患者未记录到特征性的EMG模式。
血管活性药物治疗停药后面神经麻痹延迟出现，提示神经微循环障碍是主要的病理生理特征。根据术中EMG活动可分为两组。在一组出现“A波群”的患者中，药物治疗显然掩盖了术后立即出现的面神经功能缺损。4例未出现“A波群”的患者在血管活性药物治疗期间未发生典型的迟发性面神经麻痹，而是在此之后发生。治疗终止与迟发性麻痹发作之间的时间间隔提示改善的微循环具有保护作用。
