In the past, I often heard the old man say, “The left eye jumps for money, the right eye jumps for disaster”. In our daily life, we often encounter the situation of involuntary eyelid jumping. In most cases, the involuntary jumping of the eyelids often stops quickly and does not affect life. However, there are some people whose involuntary eyelid jumping will exist intermittently for a long time, and even gradually extend to the whole half of the face, causing twitching of the corners of the mouth. In severe cases, it may even affect the vision of the same side of the eye. At this point the eyelid twitching is not indifferent and is medically referred to as facial muscle spasm. This requires a visit to the hospital. Because the cause of the eyelid fluttering is a problem with the facial nerve, it is important to go to neurosurgery rather than ophthalmology during the consultation. Facial myoclonus is a painless, intermittent, involuntary, and irregular episode of muscle tonicity or clonus in the area innervated by the ipsilateral facial nerve (around the ipsilateral eyelid and around the ipsilateral corner of the mouth). In the early stages of the disease, the twitching is mostly intermittent in the orbicularis oculi muscle, manifested as involuntary jumping of the eyelid, and then gradually spreads to other muscles on one side of the face, and the twitching increases when nervous or excited, and stops when calm or asleep. Etiology of facial muscle spasm Clinically, facial muscle spasm is divided into two categories: primary and secondary. Secondary facial myoclonus refers to those with a clear etiology, such as various occupying lesions in the pontocerebellar horn region, inflammatory lesions, aneurysms, or traumatic damage to the facial nerve, as well as some systemic diseases such as multiple sclerosis, which cause facial myoclonus. Because the exact cause of most facial myasthenia could not be found clinically before the theory of neurovascular compression was proposed, and the imaging technology at that time could not provide an objective basis, these facial myasthenia were collectively referred to as primary facial myasthenia. Although the pathogenesis of primary facial myospasm is still controversial, because of the good results of microvascular decompression, it is gradually believed that vascular compression is the main cause of facial myospasm. Treatment methods for facial myospasm Currently, clinically common treatments for facial myospasm include drugs, acupuncture, physiotherapy, herbal medicine and local closure of facial nerve, surgery, etc. These methods can be grouped into two main categories: medical treatment and surgery. Drug treatment mostly uses sedatives, anticholinergic and antiepileptic drugs, etc., which are useful for patients with early onset or mild symptoms, but often ineffective for patients with severe spasticity. The biggest drawback is that it can only temporarily relieve or reduce the symptoms of spasticity, but cannot completely cure it, and it is difficult to be widely used for a long time because it is easy to damage the liver and kidney function and hematopoietic system at higher doses, and there is a possibility of allergy. Most of the facial nerve closure procedures use local injection of botulinum toxin type A. This method is to completely sacrifice the motor function of the muscles at the injection site, and although the spasm symptoms can be relieved after injection, the motor deficiency of the facial muscles cannot be preserved. Generally, the validity period is three months, and re-injection is still effective after recurrence. Multiple repeated injections can cause partial weakness or even permanent paralysis of the cheek muscles. In recent years, with the development of microsurgery, microvascular decompression with its extremely high surgical efficiency (>90%) and relatively small surgical risk has made microvascular decompression rapidly replace the previous treatment measures as the preferred option for the treatment of facial muscle spasm. After microvascular decompression of the facial nerve, the patient’s facial spasm is relieved in the long term while the motor function of the face is generally not affected. Since 2007, our department has successfully relieved hundreds of patients from the pain of facial muscle spasm by performing facial nerve microvascular decompression.