What is facial muscle spasm
Facial myoclonus, also known as facial muscle twitching and lateral facial myoclonus, is an episodic, rhythmic, involuntary twitching of one side of the face. The twitching usually starts on one eyelid, and then gradually increases to the face and corners of the mouth, and in severe cases may involve the ipsilateral neck. The incidence of the disease is 1 per 100,000, mostly in middle-aged and elderly people, more in women than in men, and more on the left side.
Etiology of facial muscle spasm
In terms of the causative mechanism, the “nerve short circuit” theory is now recognized by clinicians, based on the fact that the intracranial facial nerve is compressed by the abnormal vasculature of the vertebrobasilar artery system in the brainstem, and the facial nerve is pathologically stimulated to produce abnormal nerve impulses, resulting in facial muscle twitching. The cause of vascular compression of the facial nerve is currently unknown. Possible risk factors are known to include advanced age, hypertension, atherosclerosis, small posterior cranial fossa volume, and genetics. In rare cases, facial myoclonus can occur secondary to intracranial tumors, aneurysms, arteriovenous malformations, brainstem lesions, and bony lesions, the chance of which is much less than 1%.
Clinical manifestations of facial muscle spasm
The twitching mostly starts from around the eyes and gradually expands downward, affecting the perioral and facial expression muscles, and in severe cases, it may involve the ipsilateral neck muscles. There are no positive neurological signs. In some cases, peripheral facial palsy can be caused by long-term illness or botulinum toxin injection.
How to confirm the diagnosis of facial spasm
Patient history, typical manifestations during attacks.
Imaging tests such as cranial CT and MRI to exclude the possibility of secondary intracranial tumors.
No history of trauma to the skull base or facial facial nerve.
No history of facial paralysis or paresis before the onset of the disease.
What is the current status of treatment for facial spasm?
Drugs, acupuncture, physiotherapy and other treatment methods are definitely ineffective. Nerve block treatment is to block the conduction function of the facial nerve using botulinum toxin and other drug injections, so that the facial muscle spasm is released. After the injection, the nerve conduction is blocked and the facial muscle becomes paralyzed or incompletely paralyzed immediately, but the facial muscle paralysis can recover within a few months and the facial muscle spasm then recurs. Therefore, the effect of Botox is short-lived, and most patients relapse in about 3-6 months, requiring re-injection. Common complications include facial palsy, dry eyes, diplopia, and difficulty swallowing. Irrecoverable facial paralysis can occur after repeated Botox injections, or resistance to Botox may develop and become ineffective.
The main hazards of facial muscle spasm
Facial muscle spasm affects the patient’s appearance and causes inconvenience to daily life and work. Irrecoverable facial paralysis can occur after repeated incorrect treatment. Facial myospasm itself is not lethal or disabling, and there is no possibility of self-healing.
Microvascular decompression provides a new way to treat facial myospasm
Microvascular decompression is the only known cure for facial myasthenia. Microvascular decompression was pioneered by an American neurosurgeon in the late 1960s. The procedure involves pushing away and fixing the blood vessels located at the root of the facial nerve that are abnormal and causing compression to the facial nerve under a surgical microscope, so that the blood vessels do not touch the facial nerve, thereby relieving the compression of the facial nerve root, restoring the normal function of the facial nerve, and making the facial muscle twitches disappear. With the improvement of this surgical technique, especially its minimally invasive, high safety, remarkable effect, low recurrence rate and low complication rate, especially the ability to completely preserve the function of blood vessels and nerves, it was soon accepted by neurosurgeons all over the world and was promoted worldwide, becoming the most effective treatment for facial muscle spasm. In addition, microvascular decompression has also been successfully used to treat trigeminal neuralgia, glossopharyngeal neuralgia, as well as intractable vertigo, tinnitus, neurogenic hypertension, and spastic diastasis.
How is microvascular decompression performed?
General or local anesthesia. The surgical incision is made in the hairline behind the ear, approximately 3 cm long, and the skin is incised and a microbony hole (the size of a locking hole, usually 1.5 cm in diameter) is drilled in the skull to enter the skull. The facial nerve root is explored, and the responsible vessel compressing the facial nerve is carefully identified. After the responsible vessel is fully freed by sharp stripping method, it is pushed away from the facial nerve and fully decompressed, and a decompression pad of suitable size and shape is placed between the responsible vessel and the brainstem to prevent the recurrence of compression. The entire procedure is performed under a microscope.
Surgical results of microvascular decompression
For experienced neurosurgeons, the overall efficiency of microvascular decompression for facial myospasm can be more than 98%, and there are two types of effective patients: 2/3 patients have immediate disappearance of postoperative myospasm, and 1/3 patients still have postoperative myospasm, but it will disappear within 2 weeks-12 months, which is called delayed cure. Ineffectiveness is 2-3%, and ineffectiveness may be due to tight adhesion of the vessel to the nerve that cannot be separated or missing the responsible vessel. There is a 2-3% recurrence rate after surgery, which may be caused by the new appearance of the responsible vessel compressing the facial nerve again, and the recurrence is treated effectively with another surgery.