Facial muscle spasm, also known as facial twitching, manifests as paroxysmal involuntary twitching of the hemifacial muscles.
Epidemiology
Most patients develop the disease after middle age, with more females in 10,000. The prevalence rate is 7.4/100,000 for men and 14.5/100,000 for women.
Causes of morbidity
Compression of facial nerve roots by sclerotic or ectopic intracerebral vessels, causing demyelination of facial nerve roots, is the main cause of facial muscle spasms
Pathogenesis
There are two main theories.
The peripheral theory suggests that the compression of nerve roots by blood vessels squeezes nerve fibers together, causing pseudosynaptic formation between adjacent nerve fibers, resulting in a “short circuit” and causing facial muscle spasm.
The central theory suggests that the main cause of facial muscle spasm is the increased excitability of the facial nucleus, and the normal afferent impulses become efferent impulses via the facial nucleus, causing facial muscle spasm.
Clinical manifestations
Facial myospasm is located in the innervated area of the facial nerve and can affect all five branches.
The typical facial spasm begins with twitching of the orbicularis oculi muscle and gradually involves the other muscles of the face and, in severe cases, the ipsilateral neck muscles, the vastus cervicis.
The degree of spasm varies and can be aggravated by fatigue, tension and voluntary movements, and the spasm stops after falling asleep. Some patients may experience mild facial pain, headache and/or tinnitus during spasm attacks, and some patients with longer duration of the disease may experience mild facial muscle paralysis.
Conservative treatment
Medication: The treatment drugs include carbamazepine and Toltea, but they are not as effective as trigeminal neuralgia
Conservative treatments such as massage, physical therapy and acupuncture are inaccurate and are not recommended.
Botulinum toxin type A local injection treatment: Botulinum toxin type A consists of a single polypeptide chain, which inhibits the quantum release of acetylcholine through enzymatic effect, causing the muscle contraction to be weakened and reducing facial muscle spasm.
The common features of these means are their short validity, the lack of targeting of the cause and the need for repeated treatments. The latter even comes at the expense of the function of the facial nerve
Surgical treatment
1. Indications for surgery
Patients with a history of more than 1 year, whose conservative treatment is ineffective and whose physical condition can tolerate anesthesia for surgery.
2.Commonly used surgical methods
The above treatment can only obtain short-term effect, and surgery can obtain more lasting effect.
(1) Facial nerve trunk or branch amputation: This surgery destroys the conduction function of the facial nerve and replaces spasticity with facial nerve paralysis. Due to nerve regeneration, facial muscle paralysis is restored 3~5 months after surgery and spasticity recurs; this procedure is rarely used clinically.
(2) Facial nerve root microvascular decompression: Because vascular compression of the facial nerve root is the main cause of facial muscle spasm, facial muscle spasm can be stopped by surgically separating the blood vessel from the nerve. Preoperative examination can clarify the cause of facial muscle spasm. The procedure is minimally invasive craniotomy, the length of the surgical incision is about 4cm, the surgical bleeding is only tens of ml, and the operation time is about 2 hours.
Within 1 year after surgery, 90-95% of the patients’ symptoms completely disappear, the recurrence rate is very low, and surgical complications are rare, about 3% of the patients have different degrees of hearing impairment after surgery.
Because of its high efficiency and low recurrence rate, it has become the preferred surgical treatment for facial muscle spasm at present.
The expert team has experience in hundreds of these types of surgeries.