Facial spasm (hemifacial spasm HFS) is a variety of causes of facial nerve ectopic impulse distribution, causing paroxysmal hemifacial muscle involuntary twitching, the onset of the patient’s appearance, causing greater physical and psychological pain to patients. It is believed that most of the spasms are caused by the compression of the facial nerve root exit zone (REZ) by the pulsating blood vessels, resulting in local demyelination, nerve fiber contact conduction and overexcitation. Arachnoid adhesions caused by various inflammatory diseases, compression and wrapping of local nerves, sequelae of facial neuritis, and tumor compression of nerves in the pontocerebellar horn region are rare. There are two hypotheses for the cause of the disease: (1) myelin sheath is damaged after vascular compression of the facial nerve, and ectopic impulses are generated by trans-synaptic transmission between nerve fibers; (2) vascular compression is similar to the “ignition” mechanism, resulting in increased excitability of the motor nucleus of the facial nerve. The results of animal experiments suggest that increased excitability of the facial nerve motor nucleus may be the main pathophysiological basis for the development of HFS[i] II. Anatomical basis Rhoton[ii] divided the vascular nerve complex in the CPA into three pairs of vascular nerve complexes: upper, middle and lower. The superior vascular nerve complex mainly includes the trigeminal nerve and the associated superior cerebellar atery (SCA) and the midbrain, midbrain cerebellar fissure, superior cerebellar peduncle, and inferior surface of the cerebellum; the middle vascular nerve complex mainly includes the facial auditory nerve and the associated anterior inferior cerebellar atery (AICA) and the pontocerebellum, mid cerebellar peduncle, pontocerebellar fissure, and cerebellar The inferior vascular-neural complex mainly includes the glossopharyngeal nerve, vagus nerve, paramedian nerve and hypoglossal nerve and posterior inferior cerebellar artery (PICA) and medulla oblongata, inferior cerebellar peduncle, medulla oblongata cerebellar fissure, and inferior occipital part of cerebellum. Zhang Qinghua, Zhang Li et al [iii] applied 15 national adult cranial wet specimens adequately fixed with 10% formaldehyde and filled with latex, and dissected, observed, measured and photographed the vascular-neural complex in the CPA area layer by layer under a 4- to 25-fold surgical microscope via a suboccipital lateral cerebellar approach. It provided us with valuable visual images. And the complex relationship between the facial nerve and the anterior inferior cerebellar artery (AICA) in the mid-vascular nerve complex was described in detail. III. Examination and preoperative evaluation of patients with facial myoclonus Conventional CT and MRI examinations were difficult to clarify the cause of facial myoclonus. Facial nerve examination of patients with facial myoclonus using magnetic resonance tomography angiography (MRTA) technique revealed the presence of tortuous vessels compressing the nerve near the REZ of the affected facial nerve. The sensitivity was 94.3% and the specificity was 94.1% [iv]. 1 mm thin layer scans were used for MRTA imaging, and in addition to cross-sectional and coronal scans, left and right oblique sagittal scans were performed in the same direction as the facial nerve, which clearly showed the relationship between the compressed responsible vessels and the facial nerve. MRTA examination method: On the GE 1.5Tesla MRI machine, the three-dimensional time-flight effect was used.