Facial twitching

Introduction Facial muscle twitching, also known as hemifacial spasm, is a common clinical manifestation of patients with primary facial muscle twitching. Most of them start after middle age, and more women. When the disease starts, it is mostly intermittent twitching of the orbicularis muscle, which gradually spreads slowly to other facial muscles on one side of the face. The twitching of the horn muscles is most noticeable, and in severe cases, the platysma can be involved in the same side. The degree of convulsions varies, and can be exacerbated by fatigue, mental stress, and autonomous movement, but cannot be imitated or controlled by oneself. After going to sleep, convulsions stop. It is rare to have twitching on both sides of the muscles. If there is, it is often the side that is affected before the other side. A small number of patients have mild facial pain during convulsions, and some cases may be accompanied by headaches and sick side tinnitus. Neurological examination, except for paroxysmal convulsions of facial muscles, no other positive signs were found. A small number of cases may be associated with mild paralysis of the lateral muscles in the later stages of the disease.

Cause

According to the cause, the disease can be divided into two types: special and secondary. Secondary symptoms are also called symptomatic hemifacial spasm, and any compression irritant lesion can induce this disease in the entire passage from the cerebral cortex to the peripheral branch of the facial nerve. Clinically common such as middle ear mastoid inflammation and tumors, space-occupying lesions of cerebellopontine angle (cholesteatoma and acoustic neuroma) and encephalitis, arachnoiditis, multiple sclerosis, Paget's disease and cranial depression. Those who can't find the inducement are collectively referred to as idiopathic sputum, accounting for about 2/3 of the total number of cases. In 1966, Jannetta proposed that the facial nerve is at the root of the brain (REZ) and is compressed by the small arteries that form the hemifacial spasm. The main cause, and the use of microvascular decompression treatment, achieved satisfactory results.

Jannetta suggested that the facial nerves (REZ) are compressed by the small arteries that are running, which are the main causes of hemifacial spasm. These blood vessels have anterior and posterior inferior cerebellum and varicose veins. After middle-aged people, these normal and nerve-cross-pressed blood vessels begin to harden, and blood pressure rises. Long-term compression of nerves can cause demyelinating degeneration, causing a string of electricity between the axons, and the excitement is transmitted from the passage to the afferent. There may be a large amount of abnormal potential accumulation and release, which may cause episodes of spasm. This argument can also be used to explain the causes of trigeminal neuralgia and glossopharyngeal neuralgia. However, in recent years, many scholars have held negative opinions because there are many facial nerves that are oppressed by blood vessels and no hemifacial spasm, and 20% to 30% of patients with hemifacial spasm cannot detect nerve compression. In recent years, the authors have measured serum and cerebrospinal fluid microtin in 30 patients, and found that all patients have significantly reduced serum calcium and magnesium ions, showing vascular compression nerve demyelination, which must be stimulated in the environment of reduced calcium and magnesium ions. Get rid of the disease.

an examination

Related inspection

Anti-AchR receptor antibody (anti-AchR) Brain ultrasound examination of amniotic fluid alpha-fetoprotein (AFP) Positron emission computed tomography (PET) Cerebrospinal fluid lactate dehydrogenase

Medical examination

In addition to facial muscle twitching, pay attention to the presence of facial muscle atrophy and other signs of brain nerves (such as trigeminal, auditory nerve, etc.). Typical convulsions, without other positive neurological signs, general diagnosis is not difficult. Electroencephalography and electromyography should be performed routinely. If necessary, mastoid, skull X-ray, head CT and MRI should be performed to exclude mastoid and skull diseases. It is characterized by electrical stimulation of the supraorbital nerve of the affected side, and the contraction of the muscles of the affected side of the orbicularis and other facial nerves. Normal or other diseases stimulate the unilateral supraorbital nerve, which only causes contraction of the orbicularis muscles that innervate the unilateral supraorbital nerve.

Differential diagnosis

Clinically, it should be differentiated from the following diseases:

1. Facial paralysis of facial paralysis: In the past, there was a significant history of facial paralysis. Due to the incomplete recovery of facial paralysis, the axonal regeneration was caused by confusion. The affected side left different degrees of facial muscle weakness and paralysis.

2. Idiopathic spasm: bilateral orbital tendon, often accompanied by mental disorders, EMG shows that the facial muscles are not synchronized discharge, the frequency is normal, may be caused by dysfunction of the pyramidal system.

3. Facial muscle twitch: for the facial muscles, the individual muscle bundles are slightly vibrating, often invading the surrounding orbital muscles, mostly limited to one side, can be relieved by themselves, may be caused by benign lesions of the brain stem and cranial nerve.

4. Habitual sputum: for small sputum, facial muscles have no purpose stereotypes or repeated beating, more common in one side, mostly in childhood.

5. The movement of the hand and foot caused by lesions in the midbrain and cone system.

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