Hemifacial spasm is a cranial nerve disorder in which the facial nerve is repeatedly and abnormally excited for short periods of time, resulting in involuntary spasmodic twitching of the facial expression muscles. Paroxysmal expression muscle spasm usually occurs on one side of the face, but rarely occurs bilaterally, hence the name hemifacial spasm.
The typical hemifacial spasm begins in the orbicularis oculi muscle on one side of the face and starts as a paroxysmal twitching of the eyelid, which gradually worsens and expands, spreading from the initial lower eyelid to all the muscles around the eye and then to the cheek. The rapid twitching (several times per second) of the periocular and cheek muscles during the attack causes muscle spasms that narrow the eye fissures and tilt the corners of the mouth to the diseased side for a few seconds to tens of seconds, and then resolve on their own. Some patients may have spasm of the tympanic membrane tensor muscle with tinnitus and hearing loss. Patients who have been treated with acupuncture, drug injections, etc. may have more pronounced weakness or paralysis of the facial expression muscles.
Patients with untreated facial spasm may also experience spontaneous mild to severe fluctuations in symptoms, but the overall trend of their natural course is one of progressive worsening. When the spasm extends from the orbicularis oris muscle to other muscle groups such as the buccal muscle, there are few cases in which the condition resolves on its own. Spasms of the orbicularis oculi can cause one eyelid to close, preventing daily activities such as reading and driving a car. Frequent episodes of spasticity cause severe psychological stress and fear of attending social events and public appearances, which interferes with normal life.
On physical examination, patients may be observed to have paroxysmal spasmodic twitching of one side of the facial expression muscles, and some patients may have hearing loss and mild facial paralysis on the affected side. The diagnosis can be established based on the typical history and clinical presentation. CT or MR scans of the pontocerebellar horn are performed as routine preoperative examinations with the primary goal of excluding secondary facial tics due to occupying lesions in the pontocerebellar horn. High-definition thin-layer MR scans can clearly identify whether there is vascular compression at the facial nerve root and the alignment and diameter of the compressed vessels before surgery, which is a guideline for surgery and can be used when available.
Electromyography of facial expression muscles can help in differential diagnosis. The EMG of patients with facial spasm is characterized by the rhythmic appearance of burst discharges with a frequency of 5-20 times per second, as well as single and longer duration burst discharges, the latter of which can be as high as 150-250 times per second. These electromyographic manifestations are highly pathognomonic and can establish the diagnosis on this basis.
The etiology of facial myoclonus has been the subject of much speculation and debate. The earliest documented case of facial myoclonus in the Western medical literature was an autopsy finding of an aneurysm of the left vertebral artery. However, the majority of patients seen clinically have an insidious onset, with no tumor or other etiology, and are referred to as primary (idiopathic) facial myasthenia. There is now a consensus among most neurosurgeons that the vessels that travel near the facial nerve roots (mainly the anterior inferior cerebellar artery, posterior inferior cerebellar artery, and vertebral artery) gradually become more tortuous and elongated with age, causing compression of the facial nerve roots. This pulsatile compression, when it reaches a certain intensity and lasts long enough, can lead to increased excitability of the facial nerve, resulting in facial muscle spasm.
Surgical release of the vascular compression of the facial nerve root can result in a permanent cure of facial muscle spasm. Microvascular decompression of the facial nerve root is the only known treatment that can eradicate the cause of the disease and completely cure facial muscle spasm without causing neurological dysfunction, with an efficiency of over 90%. This chapter describes this procedure in detail based on our clinical experience.
I. Anatomy of the facial nerve and the pontocerebellar horn
The somatic motor nucleus of the facial nerve that governs the facial expression muscle is innervated by the central prefrontal motor area of the frontal lobe of the brain, and its neuronal cell is located in the ventral medial part of the trigeminal spinal tract, in the anterior reticular formation of the lower pontocerebellum. (auditory nerve) and the vestibular nerve emanates from the brainstem medially above the site. The roots of the facial nerve pass dorsolaterally in front of the cerebellar vermis, followed by the lateral foramen of the fourth ventricle (Lucka’s foramen) and the choroid plexus exposed from the foramen, and laterally below by the root filaments of the glossopharyngeal and vagus nerves. The facial nerve emanates from the brainstem and accompanies the auditory nerve medially, travels anterolaterally in the subarachnoid space of the pontocerebellar horn pool, and enters the internal auditory meatus, with the length of the facial nerve in the brain pool segment being about 12-14 mm. The vertebral artery, posterior inferior cerebellar artery, and anterior inferior cerebellar artery all pass lateral to the brainstem near the facial nerve root and send out penetrating branches to nourish the brainstem, and in most cases the anterior inferior cerebellar artery sends a slender internal auditory artery to accompany the facial auditory nerve into the internal auditory meatus. This anatomical proximity makes the anterior inferior cerebellar artery the most frequent artery in the facial nerve root, and when the vertebral artery is tortuous and elongated, the posterior inferior cerebellar artery also moves up and elongates, and can compress the facial nerve root. (Figure 1)
Injuries to small arterial penetrations can lead to small foci of infarction in the brainstem, showing neurological impairment, and injury or severe spasm of the internal auditory artery can lead to hearing impairment. Therefore, the surgeon is required to be very familiar with the local anatomy of this region and to have skillful microsurgery skills.
II. Indications for surgery
Patients with primary facial spasm who are in good general health and have a strong therapeutic requirement are indications for facial nerve manifestation microvascular decompression treatment.
The disease is limited to the dysfunction of the expression muscles and does not cause other damage or endanger life. Patients with serious systemic diseases affecting anesthesia and surgery, such as uncontrolled hypertension, coronary artery disease, diabetes mellitus, abnormal liver and kidney function, and impaired coagulation mechanisms, should not undergo surgery because the risk of surgery will be greatly increased, and treatment of facial myospasm should be considered after the systemic diseases have been properly treated.
III. Pre-surgical preparation
Routine examination before surgery to exclude major systemic diseases affecting surgery. The afternoon of the day before surgery, the hair is shaved behind the ear at the occipital area, with the upper border to the level of the upper edge of the auricle and the back to the midline of the occipital area. The remaining area of hair is cleaned. Laxative leaves are taken orally and the stool is purged that evening and in the morning of the day of surgery.
Fasting in the early morning of the day of surgery and indwelling catheterization. Pre-operative medication is given according to the anesthesiologist’s medical advice.
IV. Surgical methods
1. Anesthesia and monitoring
Tracheal intubation, intravenous compound general anesthesia and indwelling catheterization are always used. The advantage is that it is safe, painless for the patient, and the surgical operation is not disturbed.
For monitoring brainstem auditory evoked potentials, stimulating earphones are placed in the affected external ear canal, and reference electrodes and detection electrodes are placed in the forehead and earlobe, respectively, to determine the basal value of brainstem auditory evoked potentials before the start of surgery after the anesthesia has stabilized.
2. Body position
The patient is placed in a lateral position with the affected side upward, the upper body elevated about 15 degrees, and the head naturally drops about 15 degrees, with the mastoid process at the highest level of the head and 5-10 cm above the level of the atrium to keep the intracranial venous sinus at a low pressure and avoid cerebellar swelling. The shoulder on the affected side is gently pulled toward the caudal end of the bed with a shoulder strap so that the operative field is not affected by the shoulder, and care is taken not to pull too hard to avoid injury to the brachial plexus nerve (Figure 2).
3.Surgical incision and bone window position
A straight or transverse incision of approximately 4 cm in length is made in the center of the posterior hairline of the affected mastoid notch, according to the operator’s custom (Figure 3). After local infiltration with epinephrine saline (1:200,000), the skin and subcutaneous tissues were incised and the skin margin was hemostatic with bipolar electrocoagulation. The occipital muscles are incised with an electric knife up to the skull, and the muscles around the occipital and mastoid notches are peeled and retracted. The mastoid process is often connected to the sigmoid sinus by 1-2 patent foramen ovale posteriorly, and the patent foramen ovale is closed with bone wax. The bony hole is drilled posterior to the mastoid notch and enlarged with an occlusal forceps into a circular window 2-2.5 cm in diameter, laterally to the posterior border of the sigmoid sinus and inferiorly to the point where the occipital bone thins and begins to curve anteriorly at the base of the posterior cranial fossa.
In patients with large mastoid airspace, it is often necessary to bite open the mastoid airspace to obtain satisfactory exposure, and bone wax should be used to carefully close the mastoid airspace to avoid cerebrospinal fluid leakage after surgery. Before biting off the skull, the dura mater should be freed well, so as not to injure the dura mater and venous sinuses. The guiding vein should be properly electrocoagulated to stop bleeding when encountered.
Bone wax is used to close the bone window margin, and the skin incision and muscles are protected with wet cotton sheets to prevent air from entering through the vein to form an air embolism. The dura is incised in the shape of an escapement, with the middle one pointing laterally and a needle dangling from each corner of the dura. (Figure 4)
4. Reveal the facial nerve root and responsible vessels
Place the operating microscope, cover the surface of the cerebellum with a brain swab to protect the cerebellum, gently retract the cerebellar hemisphere medially with a brain press under the direct view of the operating microscope, reveal the arachnoid membrane in the pontocerebellar horn pool and cut it open, and slowly release the cerebrospinal fluid until the cerebellum collapses inward due to gravity and can be easily retracted inward and upward. The jugular foramen and the posterior group of cranial nerves exiting through it are explored and located. The pontine vein (inferior rock vein) is often encountered near the jugular foramen confluent with the dural sinus and can be cut after electrocoagulation if it interferes with the surgical exposure. The arachnoid membrane is sharply cut and the cerebellum is further stretched to increase the exposure of the posterior group of cranial nerves. Identify the linguopharyngeal nerve root, usually a separate one located cephalad from the vagus and collateral nerves, and continue to sharply dissect the arachnoid between the nerve and the cerebellum along the dorsal (superior) side of the posterior group of cranial nerves anteriorly and medially. Do not attempt to identify the facial and auditory nerves at the opening of the internal auditory canal at this time, and do not expose the facial nerve root along the distal end of the facial nerve toward the brainstem; this anatomic excursion increases the risk of auditory nerve injury. To sharply detach the arachnoid superior to the glossopharyngeal nerve, gently lift the cerebellum and reveal it medially; the choroid plexus extending from the lateral saphenous fossa of the fourth ventricle can soon be seen, and the area of the facial and auditory nerves exiting and entering the brainstem can be revealed by lifting it. The facial nerve can be seen anterior to the medial aspect of the auditory nerve, and its root exiting the brainstem is located medial to the root of the auditory nerve (closer to the medulla oblongata) and is slightly more gray in color than the pure white auditory nerve; this area is where the facial nerve exits the brainstem (REZ zone). (Figure 5)
5. Treatment of the responsible vessels
Professor Rhoton from the United States summarized the common forms of arterial compression of the facial nerve root in his neuroanatomical study (Figure 6). According to our statistics of 1200 surgeries, the responsible vessels compressing the facial nerve were the anterior inferior cerebellar artery in 511 cases (42.6%); the posterior inferior cerebellar artery in 255 cases (21.3%); the anterior inferior cerebellar artery + posterior inferior cerebellar artery in 154 cases ( 12.8%); anterior inferior cerebellar artery + vertebral artery in 115 cases (9.6%); posterior inferior cerebellar artery + vertebral artery in 88 cases (7.3%); anterior inferior cerebellar artery + posterior inferior cerebellar artery + vertebral artery in 77 cases (6.4%). When the vertebral artery is involved in the joint formation of compression, it leads to the most severe spasticity symptoms, difficult surgical management, and prone to complications such as hearing impairment and vertigo. The anterior inferior cerebellar artery can form arterial loops posteriorly to compress the facial nerve root and then turn laterally or inferiorly; the posterior inferior cerebellar artery can also meander upward to form arterial loops to compress this area before its journey toward the posterior lateral cerebellum; the laterally meandering and thickened vertebral artery can push the aforementioned arterial branches onto the brainstem, increasing the compression of the facial nerve root and causing difficulty in free decompression.
After the responsible vessel is found, it should be carefully freed from the nerve root and the nearby brainstem to release the compression of the vessel on the brainstem and nerve root and relocate it to a site where it will not fold at an angle and the nerve will not be compressed. Often, small arterial branches enter the brainstem from the responsible vessel, preventing the free displacement of the responsible vessel, and attention must always be paid to the possibility of branches entering the brainstem on the medial side of the vessel, especially at the tips of arterial loops. Such branches must not be cut off by electrocoagulation, but must be carefully freed, and the responsible vessel can usually be freed and padded out a sufficient distance. Special care is taken not to directly pluck the facial and auditory nerves. A Teflon cotton ball of appropriate size is selected and placed between the vessel and the brainstem so that it can block the displaced vascular loop from returning to its original position of compression. Remember to tear it loose into a cotton ball shape, sheet-like Teflon pads are easily dislodged and poorly isolated. teflon cotton pellets are soft and easy to place, but also pay attention to the size of the pad entry, too large and too small can affect the surgical result, do not make the Teflon cotton directly contact the facial nerve root, and do not pose pressure on the nearby cranial nerves and brainstem. (See Figure 5)
We do not advocate the so-called “combing” of the facial nerve trunk. Combing can only result in damage to the facial nerve, leading to paralysis of the facial expression muscles for a long or short period of time after surgery.
Many surgeons also use other implants, such as Ivalon sponges, artificial dura mater, polyester vascular patches, etc. The key to successful surgery is to displace the responsible vessels and keep them from returning. The use of absorbable materials such as gelatin sponges and muscle sheets should be avoided because the responsible vessel may return to its original position of compression. Bringing the artery back into contact with the nerve and causing a recurrence of facial spasm.
The tortuous elongated and thickened vertebral artery often causes difficulties in freeing the vessel for decompression. We use freeing the vertebral artery in such patients by wrapping it with Teflon cotton or polyester vascular patch and then moving it posteriorly and laterally and adhering it to the lateral wall of the posterior cranial fossa with bioadhesive. This method is better than directly inserting Teflon cotton between the vertebral artery and the brainstem, with complete decompression of the facial nerve root and no new compression of the brainstem. It should be noted that in patients with tortuous vertebral artery compressing the facial nerve root, there are usually anterior inferior cerebellar artery or posterior inferior artery jointly involved in forming the compression, so these branch arteries should be free and padded together, and there should be no direct contact between the passing artery and the REZ of the facial nerve in the vicinity.
6. Intraoperative electrophysiological monitoring
Intraoperative monitoring of the facial nerve (facial electromyography) and auditory nerve (brainstem auditory evoked potentials) is helpful for surgery and allows the operator to detect in a timely manner whether there is excessive strain resulting in injury to the facial auditory nerve and inadequate blood supply to the inner ear (spasm of the internal auditory artery). Currently, we mainly use brainstem auditory evoked potentials to monitor the auditory nerve for intraoperative injury. After induction of anesthesia, a stimulation headset is placed in the external ear canal on the operative side, a reference electrode is placed in the forehead between the eyebrows, and a detection electrode is placed under the occiput or in the earlobe. A 5- to 10-Hz acoustic signal stimulation was used, superimposed 1000 times, and the amplitude and latency of each wave of the underlying auditory evoked potential were measured before the start of the procedure. The waves were monitored repeatedly during the process of revealing the facial nerve and dealing with the responsible vessels, and compared with the preoperative wave amplitude and latency. If the V-wave amplitude on the brainstem auditory evoked potentials decreases and the latency period is prolonged, the operation should be performed with extra care. If the V-wave amplitude decreases by 75% and the latency is prolonged by 1 ms, the operation should be stopped and the cause of the waveform change should be investigated. After eliminating the causes of electrode loosening and displacement and deep anesthesia, pay attention to whether there is excessive strain on the auditory nerve and brainstem and whether there is spasm in the internal auditory artery, etc., promptly eliminate the causes, relax the strain on the auditory nerve, apply poppy alkaline cotton tablets to the spastic internal auditory artery, and continue the operation after the evoked potential waveform has basically recovered. If the preoperative auditory evoked potential is normal, but it is significantly reduced or disappeared intraoperatively, the patient will most likely have hearing impairment after surgery.
7.Closing the incision
After satisfactory neurological decompression is achieved, the arterial loops are released from spasm by local patching with poppy base, the surgical field is flushed, and the incision is closed. The suture of the dural incision is usually difficult to achieve complete non-leakage, and we used to seal it with muscle pieces, gelatin sponge, collagen sponge, etc., but the incision cerebrospinal fluid leakage still occurred in individual patients after surgery. Now we have switched to a sutureless artificial dural patch covered with gelatin sponge, which basically eliminates the incisional cerebrospinal fluid leakage.
The muscle of the occipital area is closed subcutaneously with interrupted sutures in layers of No. 7 silk. No drainage tube or drainage strip was placed, and the skin was finally closed in full layers.
V. Surgical results
Prof. Samii from Germany reported the long-term follow-up results of 143 cases of manifest microvascular decompression for facial muscle spasm, of which 117 cases were followed up for an average of 9.4 years. 69 cases (59%) had spasm relief at discharge, and by 6 months after discharge, the number of patients with spasm cessation rose to 108 cases (92.3%), and 9 patients were ineffective or recurred.
In Japan, Goto reported 131 cases of long-term follow-up after microvascular decompression of facial myospasm, with a follow-up period of 1.5 to 10 years. 91.6% were completely cured, 3.1% improved (75% reduction in symptoms), 7 were ineffective or recurred, and 2 were cured by reoperation. 76.5% of the 102 cured patients had spasticity that stopped immediately after surgery, and the rest had spasticity that stopped 1-12 months after surgery. -The spasticity of the remaining patients stopped in 1 month after surgery. He summarized the long-term follow-up results of 4865 cases of HFS treated with MVD in 23 hospitals in Japan: 83.7% of the symptoms disappeared, 12.2% of the symptoms decreased, and only 4.1% of the surgery was ineffective.
Our hospital summarized the results of 1200 cases of surgical treatment for facial spasm in recent years. 797 cases (62.4%) had immediate disappearance of symptoms after surgery, and among 403 cases with varying degrees of facial spasticity, 305 cases had disappearance of symptoms 20-160 days after surgery. The total effective rate was 94.3%; 31 cases (2.6%) were ineffective and 38 cases (3.2%) were recurrent.
In patients whose postoperative myoclonus could not be stopped immediately, it was speculated that it might be due to the regeneration of local demyelinating lesions of the facial nerve and the repair of ultrastructural pathological changes of motor neurons that took some time to complete. In addition, the small size of the posterior cranial fossa and the insufficient free displacement of the thick blood vessels, which still partially transmits pressure to the facial nerve root through the pad cotton, may also be a reason. Delayed resolution of symptoms is defined as the persistence of posterior myasthenia gravis for more than 1 week after apparent microvascular decompression. The incidence of delayed resolution of symptoms after surgery is higher in patients with a longer history (more than 5 years) and involvement of the vertebral artery in the compression. Those who experience delayed healing tend to resolve on their own within six months postoperatively, with most of these patients resolving within 3-6 weeks postoperatively. Therefore, patients whose facial muscles still have spasticity symptoms after surgery should be explained patiently, the reasons should be explained, and follow-up should be continued for at least six months before making a judgment on the effect of surgery.
The incidence of ineffectiveness and recurrence were 2.6% and 3.2%, respectively, among 1200 cases of facial muscle spasm surgery in our hospital in recent years. According to the intraoperative findings, the causes of ineffectiveness and recurrence were summarized as follows: 1, poor exposure of the facial nerve root, incorrect judgment or omission of the responsible vessel; 2, inappropriate selection and placement of decompression materials, incomplete decompression of the facial nerve root; 3, placing too many pads or placing them on the facial nerve root, thus constituting new compression; 4, dislodgement or displacement of the pads, and repositioning of the responsible vessel; 5, the facial nerve root, and the facial nerve root. 4, the pad is dislodged or displaced and the responsible vessel is repositioned; 5, local arachnoid adhesions and new responsible vessels constitute compression. Therefore, correct determination of the responsible vessel and precise operation during surgery can improve the outcome of surgical treatment. In patients with ineffective treatment or recurrence, secondary surgical decompression is still effective, but the possibility of surgical injury to the facial nerve increases compared with the first surgery.
VI. Surgical complications
Microvascular decompression for facial spasm is a relatively safe procedure, but it still involves some of the inevitable risks of posterior cranial fossa craniotomy, including possible direct mechanical injury to the cerebellum, brainstem, and cranial nerves, as well as indirect injury caused by local vascular injury or spasm leading to impaired blood supply or hemorrhage to the cerebellum, brainstem, and cranial nerves. In the 1980s, a retrospective analysis of 450 surgeries in 16 groups reporting a total of 433 patients resulted in 71 cases (15.8%) with permanent complications, including 1 case (0.2%) of death. One patient died after surgery. At long-term follow-up, only hearing impairment was not significantly recovered, and 4 patients still had mild vertigo, while other complications did not cause long-term adverse consequences.
Hearing impairment: Hearing impairment on the operated side is the main complication of facial nerve root manifestation microvascular decompression. In some patients, the development of the mastoid atrium is large, and the mastoid atrium needs to be opened when the bone window is opened during surgery, which can lead to fluid accumulation in the atrium after surgery, resulting in the patient feeling “stuffy” in the operated side of the ear and hearing loss. As the fluid is absorbed, hearing can be fully restored in a few weeks. Another cause of hearing impairment is excessive medial stretching of the cerebellum and brainstem during exposure of the facial nerve roots, causing strain injury to the auditory nerve.
Intraoperative freeing of the responsible vessels, especially the anterior inferior cerebellar artery, can induce spasm of the internal auditory artery and inadequate blood supply to the inner ear, which is another cause of postoperative hearing impairment. In our experience, about 20% of patients complain of postoperative hearing loss, most of which recover within a few weeks to months after surgery, with only about 2% experiencing permanent hearing impairment. The position of the bone window is very important to reduce the strain on the cerebellum and brainstem, and its lateral edge must go to the posterior edge of the sigmoid sinus to minimize the strain on the cerebellum.
Intraoperative real-time brainstem auditory evoked potential monitoring can effectively reduce the incidence of hearing impairment. jannetta reported that the incidence of permanent hearing impairment was 7% before the use of intraoperative brainstem auditory evoked potential monitoring, and decreased to 0.7% after the use of intraoperative brainstem auditory evoked potential monitoring.
2. Facial palsy: about 1/4 of the patients experience varying degrees of facial weakness after surgery. It can occur immediately after waking up from anesthesia or gradually several days after surgery. Most of the patients have mild symptoms, only some of the expression muscles are weak, such as slow or slightly weak eye closure on the affected side and drooping corners of the mouth, but a few can have complete peripheral facial palsy. Most patients who undergo surgery have received various acupuncture, injections or other traumatic treatments before surgery, and these treatments can also cause irreversible facial nerve damage. Spastic episodes can partially mask the already existing mild facial palsy, while the spasticity stops after surgery and the original facial palsy becomes apparent. It is important to distinguish between facial palsy newly caused by surgery and facial palsy that existed before surgery.
Causes of facial palsy due to surgery include direct mechanical damage caused by operations such as intraoperative pulling (which occurs immediately after surgery), or surgery activates a virus inherent in the facial nerve, resulting in viral facial neuritis, similar to Bell’s palsy (postoperative delayed facial palsy), or there may be ischemic edema due to compromised blood flow to the facial nerve. In the hands of experienced surgeons, mechanical damage to the facial nerve is less likely to occur, but still the latter two causes of facial palsy cannot be completely prevented. Most facial palsy can be fully recovered within weeks to months, and only 1% of our cases have a residual permanent facial palsy of varying degrees.
3. Vertigo: A small number of patients experience severe postoperative vertigo with unstable walking, most of which gradually disappears within 1-2 weeks. 143 patients reported by Samii had 14 cases of postoperative vertigo, with an incidence of 9.6%, and 4 cases (2.7%) still had vertigo at long-term follow-up. The incidence of postoperative vertigo in our cases was about 10%, but the ones who still had vertigo in long-term follow-up were under 2%, which interfered with daily life. The possible causes of postoperative vertigo are: 1, ischemia of the inner ear vestibule due to spasm of the internal auditory artery. 2, injury of the vestibular nerve by stretching. 3, the vestibular area of the brainstem is located just near the superior lateral facial nerve root of the medulla oblongata and is affected by direct disturbance of the surgical operation. 4, compression of the vestibular area of the medulla oblongata by the vertebral artery through the pad cotton. 5, spasm or occlusion of the small artery that nourishes the vestibular area of the medulla oblongata after stretching. Intraoperative care should be taken to avoid the above factors that cause vertigo.
4, Cerebrospinal fluid leakage: After posterior mastoid micro-osseous craniotomy, the dural incision is difficult to close tightly directly and usually needs to be repaired. If the patient’s mastoid airspace has been opened during surgery and not closed tightly with bone wax, cerebrospinal fluid can leak out through the eustachian tube. If the postauricular incision is not sutured tightly enough, cerebrospinal fluid leakage from the incision can occur. After taking these measures, the incidence of postoperative cerebrospinal fluid leakage in our hospital is less than 2%.
5, intracranial infection: mostly occurs 3-4 days after surgery, the patient’s headache worsens, the body temperature rises, and the leukocyte count of lumbar puncture cerebrospinal fluid increases. The incidence of intracranial infection is about 1% in our hospital, which can be controlled after strengthening antimicrobial treatment (intrathecal injection if necessary). Strict intraoperative aseptic operation is the key to avoid postoperative infection.
6. Other complications: Other complications include intracerebellar hematoma, injury to other adjacent cranial nerves (mainly the glossopharyngeal nerve, vagus nerve, abducens nerve, etc.), brainstem or cerebellar infarction, subcutaneous infection of the incision, etc.
Strict intraoperative aseptic concept; avoiding excessive and prolonged brain pressure plate traction and direct instrumentation touching cranial nerves during operation; paying attention to preserving the small penetrating arteries between the responsible vessels and the nerves and brainstem, especially the internal auditory artery; and strict and meticulous closure of the incision can effectively avoid or reduce the occurrence of postoperative complications.
VII. Summary
In summary, manifest microvascular decompression is less invasive, has a high cure rate, and can completely preserve the function of normal nerves, which has become the most effective method for treating facial muscle spasm. Therefore, we currently use only one method of manifest microvascular decompression for the treatment of facial myasthenia gravis. We do not advocate that patients seek treatments such as acupuncture or injectable medications that may lead to permanent facial nerve damage, nor do we recommend that patients seek oral medications that are largely ineffective. If there is a disease that prevents surgery, the serious systemic disease should be treated first before surgery is performed to treat the facial spasm. Based on our experience over the years, apparent microvascular decompression is a fairly safe procedure with a low complication rate in the hands of experienced physicians. However, because of the dense vascularity and nerve density in the pontocerebellar horn region, the complex anatomy, and the large number of vascular variants responsible for compressing the facial nerve, the procedure may still result in accidental injury and permanent dysfunction, requiring the surgeon to have good microneurosurgical experience and familiarity with the region This requires excellent microsurgical experience and familiarity with the anatomy of the region. Therefore, although manifest microvascular decompression is highly effective, the potential benefits and risks of surgery for a nonfatal, painless condition such as facial spasm must still be carefully weighed and fully agreed with the patient and family on this matter.