Campos-Benitez Mauricio, Kaufmann Anthony M
Department of Surgery, University of Manitoba, Winnipeg, Manitoba, Canada.
J Neurosurg. 2008 Sep;109(3):416-20. doi: 10.3171/JNS/2008/109/9/0416.
It is generally accepted that hemifacial spasm (HFS) is caused by pulsatile vascular compression upon the facial nerve root exit zone. This 2-3 mm area, considered synonymous with the Obersteiner-Redlich zone, is a transition zone (TZ) between central and peripheral axonal myelination that is situated at the nerve's detachment from the pons. Further proximally, however, the facial nerve is exposed on the pontine surface and emerges from the pontomedullary sulcus. The incidence and significance of neurovascular compression upon these different segments of the facial nerve in patients with HFS has not been previously reported.
The nature of neurovascular compression was determined in 115 consecutive patients undergoing their first microvascular decompression (MVD) for HFS. The location of neurovascular compression was categorized to 1 of 4 anatomical portions of the facial nerve: RExP = root exit point; AS = attached segment; RDP = root detachment point that corresponds to the TZ; and CP = distal cisternal portion. The severity of compression was defined as follows: mild = contact without indentation of nerve; moderate = indentation; and severe = deviation of the nerve course. Success in alleviating HFS was documented by telephone interview conducted at least 24 months following MVD surgery.
Neurovascular compression was found in all patients, and the main culprit was the anterior inferior cerebellar artery (in 43%), posterior inferior cerebellar artery (in 31%), vertebral artery (in 23%), or a large vein (in 3%). Multiple compressing vessels were found in 38% of cases. The primary culprit location was at RExP in 10%, AS in 64%, RDP in 22%, and CP in 3%. The severity of compression was mild in 27%, moderate in 61%, and severe in 12%. Failure to alleviate HFS occurred in 9 cases, and was not related to compression location, severity, or vessel type.
The authors observed that culprit neurovascular compression was present in all cases of HFS, but situated at the RDP or Obersteiner-Redlich zone in only one-quarter of cases and rarely on the more distal facial nerve root. Since the majority of culprit compression was found more proximally on the pontine surface or even pontomedullary sulcus origin of the facial nerve, these areas must be effectively visualized to achieve consistent success in performing MVD for HFS.
一般认为,面肌痉挛(HFS)是由面神经根部出口区的搏动性血管压迫所致。这个2 - 3毫米的区域,被认为与奥伯施泰纳 - 雷德利希区同义,是中枢和外周轴突髓鞘形成之间的过渡区(TZ),位于神经从脑桥分离处。然而,在更靠近近端的位置,面神经暴露于脑桥表面并从脑桥延髓沟穿出。此前尚未报道过HFS患者面神经这些不同节段上神经血管压迫的发生率及意义。
在115例首次接受微血管减压术(MVD)治疗HFS的连续患者中确定神经血管压迫的性质。神经血管压迫的位置被归类为面神经4个解剖部位中的1个:RExP = 根部出口点;AS = 附着段;RDP = 对应于TZ的根部脱离点;CP = 远端脑池段。压迫的严重程度定义如下:轻度 = 神经接触但无压痕;中度 = 有压痕;重度 = 神经走行偏移。在MVD手术后至少24个月进行电话随访,记录缓解HFS的成功率。
所有患者均发现神经血管压迫,主要压迫血管为小脑前下动脉(43%)、小脑后下动脉(31%)、椎动脉(23%)或大静脉(3%)。38%的病例发现有多个压迫血管。主要压迫部位在RExP的占10%,AS的占64%,RDP的占22%,CP的占3%。压迫严重程度为轻度的占27%,中度的占61%,重度的占12%。9例患者HFS未缓解,且与压迫位置、严重程度或血管类型无关。
作者观察到,所有HFS病例均存在致责任神经血管压迫,但仅四分之一的病例位于RDP或奥伯施泰纳 - 雷德利希区,且很少位于面神经更远端的神经根。由于大多数致责任压迫位于面神经脑桥表面甚至脑桥延髓沟起始处的更靠近近端位置,因此在进行HFS的MVD时,必须有效观察这些区域才能持续取得成功。