Liu Jiang, Liu Peng, Zuo Ying, Xu Xiaoli, Liu Hongju, Du Rose, Yu Yanbing, Yuan Yue
Department of Neurosurgery, China-Japan Friendship Hospital, Beijing, China.
Department of Neurosurgery, Liaocheng People's Hospital, Liaocheng, China.
World Neurosurg. 2018 Aug;116:e889-e894. doi: 10.1016/j.wneu.2018.05.124. Epub 2018 May 28.
Although classical hemifacial spasm (HFS) has been attributed to an atraumatic pulsatile vascular compression around the root exit zone (REZ) of the facial nerve, rare tumor-related HFS associated with meningiomas, epidermoid tumors, lipomas, and schwannomas in the cerebellopontine angle have been reported. The exact mechanism and the necessity of microvascular decompression for tumor-induced HFS is not clear, especially for vestibular schwannomas.
We retrospectively analyzed 10 patients with vestibular schwannomas out of 5218 cases of hemifacial spasm between 2004 and 2014.
Hemifacial spasm occurred ipsilateral to the vestibular schwannoma in 9 patients and contralateral to the lesion in 1 patient. The mean follow-up period was 86 months (range, 22-140 months). All patients underwent surgery for resection of the vestibular schwannoma. Following the principle of neurovascular compression, offending vessels were found in 7 patients, no offending vessels in 2 patients, and a tumor with the displacement of brain stem contributing to contralateral facial nerve compression in 1 patient. HFS was relieved immediately postoperatively in 9 patients, whereas it improved gradually and then resolved after one month in one patient with a contralateral vestibular schwannoma.
For HFS induced by vestibular schwannomas in our study, the majority of cases are caused by a combination of tumor and vascular co-compression at the REZ. Surgical intervention resulted in resolution of symptoms. For HFS with ipsilateral vestibular schwannoma, exploration of the facial nerve root for vascular compression should be performed routinely after tumor resection. It is critical to check that no vessel is contact with the entire nerve root.
尽管经典的面肌痉挛（HFS）被认为是由于面神经根部出口区（REZ）周围无创伤性搏动性血管压迫所致，但已有报道称，在桥小脑角存在与脑膜瘤、表皮样肿瘤、脂肪瘤和神经鞘瘤相关的罕见肿瘤相关性HFS。肿瘤诱发的HFS进行微血管减压的确切机制和必要性尚不清楚，尤其是对于前庭神经鞘瘤。
我们回顾性分析了2004年至2014年间5218例面肌痉挛患者中的10例前庭神经鞘瘤患者。
9例患者的面肌痉挛发生在前庭神经鞘瘤同侧，1例发生在病变对侧。平均随访期为86个月（范围22 - 140个月）。所有患者均接受了前庭神经鞘瘤切除术。按照神经血管压迫的原则，7例患者发现有肇事血管，2例患者未发现肇事血管，1例患者的肿瘤伴有脑干移位导致对侧面神经受压。9例患者术后HFS立即缓解，而1例对侧前庭神经鞘瘤患者的HFS逐渐改善，1个月后缓解。
在我们的研究中，对于前庭神经鞘瘤诱发的HFS，大多数病例是由肿瘤和血管在REZ处共同压迫所致。手术干预可使症状缓解。对于同侧前庭神经鞘瘤伴发的HFS，肿瘤切除后应常规探查面神经根部有无血管压迫。检查整个神经根无血管接触至关重要。
