As the saying goes, “the left eye jumps for money, the right eye jumps for disaster”. In reality, there are many people “left eye” jumping for many years, but never wait until the “big money”, but because of medical detours spent a lot of money. For example, toxic patients just spent money yesterday to buy a large package of “expensive Chinese medicine”, today and to play Botox, tomorrow about acupuncture, the day after tomorrow ready to go to paste the “miracle cure” cream, the results of the money spent a lot of treatment into facial paralysis, and eyelids still continue to jump. In serious cases, the eyelids continue to throb, and half of the face jumps together, like “screwing a bun”, in the words of the patient! Although it does not hurt, it is so jumping all the time, causing a serious heart burden: leaders do not dare to meet, teachers do not dare to go on the podium, managers do not dare to interview new employees ……, because the more nervous the more jumping, a jump up offstage laughter!
In fact, whether it is the left eyelid jumping, or right eyelid jumping, occasionally jumping a few times may be related to our overwork, if a long period of recurring episodes, “neither rich, nor necessarily disaster”, but disease! So what exactly is the disease? Medically speaking, we call it facial muscle spasm.
Whether the left eyelid jumping, or right eyelid jumping, neither rich, nor disaster, this is a disease, is “facial muscle spasm”!
Here we will talk about what is facial spasm.
I. Overview
Facial muscle spasm, also known as facial muscle twitching, refers to the facial nerve innervation area of the facial muscles episodic, recurrent, involuntary twitching, mostly in adulthood, between 30 to 40 years old, most of the seizures are located unilaterally, only 0.5% of the bilateral.
Etiology and classification
1. Secondary facial spasm refers to those whose etiology is clear, such as recovery from facial nerve trauma or facial neuritis caused by peripheral facial palsy, tumor of the pontocerebellar horn or arachnoiditis at the base of the skull involving the facial nerve root.
2. Primary facial spasm refers to those whose etiology is not clear from various examinations. It is mostly believed that the facial nerve root is compressed by abnormal blood vessels in the bridge section of the brain, which causes demyelination of the nerve, resulting in current “short circuit” between nerve fibers.
Clinical manifestations
1. Chronic course, mostly confined to one side, with the right side being the most common, often occurring first in the lower eyelid, and then spreading to the corners of the mouth, other facial muscles or neck expansion muscles after 1~2 years.
2. There is no aura before the attack, and the attack is characterized by rapid and frequent muscle twitching for tens of seconds to several minutes per attack.
It can be triggered by voluntary facial movements and chewing, transient eyes or random facial expressions, and can be aggravated by emotional excitement, tension, exertion or prolonged reading time, etc., while the symptoms are reduced when resting or emotionally stable.
In severe cases, the eyelid tonic contraction causes the eye fissure to become smaller, and the corner of the mouth is continuously skewed to the side of the disease; 0.8% may be accompanied by trigeminal neuralgia, but each of the two attacks; it may also be accompanied by tinnitus and hearing loss on the affected side.
5. Physical examination of primary facial muscle spasm generally has no obvious positive signs, and a few have incomplete paralysis due to various treatments.
Four, auxiliary examination
Facial EMG can find high amplitude F and abnormal muscle response waveforms. Stimulation of the mandibular rim branch of facial nerve can induce muscle potential of orbicularis oculi muscle, and abnormal facial EMG can disappear when the blood vessels compressed on facial nerve are separated during surgery.
2. CT and MRI examination can clarify the secondary facial muscle spasm caused by occupational and organic lesions.
3. MRA can show the relationship between cerebral vessels and cerebral nerves, which is helpful for diagnosing primary facial myospasm caused by vascular compression of facial nerve.
V. Diagnosis and differential diagnosis
The clinical diagnosis can often be made based on the typical medical history and observation of facial spasm, but attention should be paid to differentiate it from the following diseases in the diagnostic process.
(1) Facial muscle twitching after facial nerve palsy Facial nerve injury or facial neuritis-induced facial nerve palsy is often accompanied by contractures or collateral movements of the paralyzed muscles during functional recovery (e.g., involuntary eye closure when opening the mouth); the facial muscles on the twitching side do not contract when performing voluntary movements (e.g., when showing the teeth), while the facial muscles on the healthy side contract normally and the corners of the mouth are skewed to the healthy side.
(2) Pontocerebellar horn lesions such as tumors and arachnoiditis, patients often show damage to adjacent cerebral nerves (VII, VIII, IX and other cerebral nerves), which can be clarified by CT and MRI examinations.
(3) Hysterical blepharospasm is common in middle-aged and older women, with spasms limited to the eyelids and bilaterally synchronized when twitching, but does not involve the facial muscles of the lower part of the face.
(4) Habitual facial twitching is common in children and young adults and is a transient forced facial movement that is bilateral; electromyography shows the presence of muscle contractions consistent with those produced during voluntary movements.
(5) Chorea and tardive dyskinesia may have involuntary facial muscle twitching, but both are bilateral and accompanied by similar involuntary movements of the extremities.
(6) Restricted epilepsy may manifest as limited twitching of the facial muscles but with increased amplitude, often involving the upper neck, upper extremities, or lateralized limbs, or a typical sequential spread of restricted seizures in the cortical motor areas; epileptic waves are visible on the EEG.
VI. Treatment
1. Treatment methods used to use alcohol closure, percutaneous puncture facial nerve radiofrequency thermocoagulation, facial nerve branch or trunk mostly severed, intracranial facial nerve extrusion, facial nerve canal nerve partial injury surgery and other destructive methods, which have been abandoned. At present, microvascular decompression of the facial nerve root has become the preferred surgical treatment method, and it is also the method with the highest cure rate and the best treatment effect.
2. The key to surgical treatment of facial nerve microvascular decompression is to clarify the responsible vessels that cause compression of the beginning segment of the facial nerve root bridge and to perform adequate decompression; spasm can be controlled immediately in more than 90% of patients, and gradually stopped in another part of patients in 1 week to 6 months or more; the main complication of surgery is hearing loss on the side of surgery, with an incidence of about 2%.
3. Botulinum toxin A closure can be maintained for 3~4 months with one injection, and can be closed again after recurrence, but permanent facial paralysis can be caused after too many closures, so extreme caution should be exercised!