Indications and key points of microvascular decompression (MVD)
According to the current pathogenesis of neurovascular conflict (NVC), microvascular decompression (MVD) refers to the surgical microscopy to push away the blood vessels located in the root of the trigeminal nerve, facial nerve and other cranial nerves that are abnormal in their course and cause compression to the cranial nerves. This method can relieve clinical symptoms by removing the compression of the vessels on the cranial nerve roots. This method is a recognized effective treatment for intracranial vascular compression syndromes, which can relieve the symptoms for a long time and preserve the nerve function to the greatest extent.
I. History of MVD
In 1929, Dandy described that the arterial vessels were in contact with the trigeminal nerve roots and compression could lead to trigeminal neuralgia (TN), Gardner and Sava expanded these theories in 1962, and suggested that releasing the compression of the facial nerve could treat facial spasm HFS. In 1967, Professor Jannatta developed these theories and introduced the concept of microvascular decompression (MVD) for the first time, while they applied MVD for the first time in patients with symptoms of cranial nerve compression, such as trigeminal neuralgia (TN), hemifacial spasm (HFS), glossopharyngeal neuralgia (GPN), neurogenic hypertension (NF), and primary vertigo, all with good results. This procedure is often referred to as Jannetta’s operation. 1981 Freckmann N et al. also achieved good results in the treatment of spasmodic torticollis (spastic tilt neck) using MVD. 1997 Ko Y [13] et al. in 1998, Samii M et al [14] also used this procedure to achieve success in a case of superior oblique myokymia (SOM). With the development of microneurosurgery, MVD has been improved and promoted, replacing the previous destructive treatment of complete or partial severance of the nerve, and has now become the preferred method for the treatment of trigeminal neuralgia and facial spasm.
Magnetic resonance (MR) and MVD
Preoperative MRI cranial nerve scan is important for guiding surgery: MRI can clearly show the relationship between neurovascular compression, which is important for diagnostic and therapeutic surgery. angiography (3D-TOF MRA) in 564 patients from 1992 to 1998, which was important in the selection of patients for surgery to predict the outcome of surgery. And intraoperative confirmation of fine artery compression and arachnoid thickening. It is clear from the above that preoperative MR examination is necessary.
The role of postoperative MR: Nagaseki Y et al. concluded that postoperative oblique sagittal gradient MR scan is a useful tool for follow-up of cases of neurovascular compression at the REZ, and Chang JW et al. also concluded that postoperative MRI can be effective for postoperative follow-up.
III. Microvascular decompression procedure
1. Indications for surgery:
Magnetic resonance imaging of the cranial nerves, showing significant vascular compression of the nerve roots in the root exit zone (REZ), further clarifies the diagnosis and provides support for the surgical treatment of MVD. At the same time, the application of advanced neurosurgical microscope and rich experience in microscopic neurosurgery ensure smooth and smooth operation, intraoperative neuroprotection and very low postoperative complication rate.
2. Indications for surgery
(1) Facial muscle spasm: twitching at the corner of one side of the eye or the corner of the mouth, which is ineffective with drug treatment.
2）Trigeminal neuralgia: lightning-like pain on one side of the face, ineffective by medication or other treatments
(3) Glossopharyngeal neuralgia: episodic pain in one side of the throat or the root of the ear, ineffective with medication
(4) spastic slanting neck: involuntary deviation of the head and neck to one side, excluding congenital slanting neck.
5) Vertigo tinnitus syndrome: severe vertigo accompanied by unilateral tinnitus and hearing loss, which affects work and life for a long time.
3. The surgical steps, with six key points, are as follows
Step 1: Patient’s position: The position of the head is crucial to provide maximum surgical space. Under general anesthesia, the patient is positioned on the healthy side, with the head dropping 15 degrees and leaning forward, the neck slightly flexed forward, the chin about two cross fingers from the sternum, and the shoulder pulled toward the hip with a bandage so that the head-neck-shoulder angle is greater than 90°. Make the affected mastoid roughly parallel to the operating table and in the highest position. (For trigeminal nerve decompression, the sagittal line of the head is kept parallel to the bed surface. In case of facial nerve or low group cranial nerve decompression, the median line of the head should be slanted downward by 15° so that the top of the head is lowered and the cranial nerve roots can be fully exposed.) . By starting with the patient’s head slightly tilted to the affected side, the cerebellum will naturally collapse due to its own gravity to form the surgical channel without traction, which facilitates the exposure of the surgical area and the application of the surgical microscope. During surgery, the head and face are rotated 10 degrees to the healthy side to facilitate keeping the optical axis of the operating microscope in line with the access.
Step 2: Surgical incision: The location of the incision varies depending on the size of the patient’s neck. The skin is prepared 3×3 cm behind the ear, recognizing important marker points such as the mastoid bulge, the diastasis muscle sulcus, and the point of the external occipital bulge, so that the operator can identify the course and junction of the transverse and sigmoid sinuses. A small 4 cm longitudinal direct skin incision is made behind the affected ear, approximately 0.5 cm inside the hairline, with the incision perpendicular to the inferior line of the collar, flattening the tip of the ear at the upper end and the earlobe at the lower end. The skin and muscles are retracted to reveal the mastoid root, and the incision is made layer by layer to reach the occipital scales. The incision is slightly shorter in patients with a long, thin neck, and slightly longer and angled inward in patients with a thick and short neck, and the oblique incision is made in the hairline at an oblique angle of 20° to 30° from 2 transverse fingers above the mastoid. Regardless of the incision used, it is required that 3/4 of the incision be located below the connection between the transverse and sigmoid sinuses and 1/4 above the connection between the transverse and sigmoid sinuses.
Step 3: Bone window: important bony landmarks, such as the diastasis muscle groove, should be fully exposed before drilling. The mastoid guiding vein is used as a good marker for the junction of the transverse and sigmoid sinuses. The upper edge of the bone window must expose the junction of the transverse and sigmoid sinuses, and the top of the bone window should reach the edge of the jugular bulb when performing facial nerve decompression. The occipital scales are drilled and a small bone window of about 3 cm in diameter is opened, with the anterior and inferior borders as close as possible to the sigmoid sinus and fully exposing the mastoid root and occipital condyle. Try not to open the mastoid airspace, otherwise the open mastoid airspace is closed with bone wax.
Step 4: Exploration of the pontocerebellar angle is the most dangerous part of the surgery and requires full patience and care. The dura is incised in a “┴” shape, the dura is cut below the transverse sinus, extended outward and downward, then folded medially, the dural flap is turned toward the midline, and additional small incisions are made in the dura at the uppermost edge near the junction of the transverse and sigmoid sinuses (pay particular attention to this point when doing trigeminal nerve decompression). The dura is suspended so that the transverse sinus is drawn as far outward and upward as possible. Before placing the microscopic instruments, the cerebellar hemispheres are protected with moistened cotton sheets and gelatin sponges and gently inserted deeper into the pontocerebellar horn to release cerebrospinal fluid, which is then seen to descend from the sella and the cerebellar curtain. The cerebrospinal fluid is aspirated under the surgical microscope, and the arachnoid is sharply cut.
Sequence of surgical operations. The posterior group of cranial nerves is treated first for the following reasons. (1) The patient’s symptoms are often caused by direct or indirect compression of the nerve by the thick and twisted vertebral basilar artery. To obtain adequate decompression, the vertebral basilar artery must be displaced downward, and to displace the vertebral basilar artery the arachnoid membrane proximal to the nerve must first be released. Therefore, the arachnoid around the posterior group of cranial nerves must first be opened and the cerebellum lifted to expose the pontine sulcus. After pushing down the vertebrobasilar artery, the directly responsible vessel can often be found in the nerve root area of the facial nerve at the pontine sulcus. ②The following situation often exists: because the vertebrobasilar artery has been sufficiently pushed away, when decompression of the facial nerve is completed, it is often possible to partially or even completely reduce the VA pressure on the trigeminal nerve, and sometimes decompression of the trigeminal nerve has even been completed. ③Another advantage of bottom-up dissection is that the posterior group of cranial nerves is usually not surrounded by rock veins that obstruct the surgical access and are prone to bleeding, and the management of rock veins is often a difficult point in MVD surgery. This operation not only provides a satisfactory surgical exposure view, but also improves surgical safety.
Exploration of the pontocerebellar paramedian area and the pontocerebellar angle ①Caudal group of cranial nerve surgery such as the lingual pharyngeal nerve is performed by using an extra-cerebellar inferior approach to retract the cerebellum and tonsil and look for 9, 10 and 11 pairs of cranial nerves and their surrounding compressed vessels at the jugular foramen. ② Facial nerve decompression exploration of the pontocerebellar angle, using the lateral cerebellar approach, because the facial nerve REZ emanating from the pontine sulcus is located on the deep side of the linguopharyngeal and vagus nerves, so the linguopharyngeal and vagus nerves should be exposed first, and the arachnoid membrane at the nerve root should be cut, and the cerebral pressure plate should be used to retract the cerebellar vermis, while adjusting the patient’s head position and the optical axis of the surgical microscope, and looking for 7 and 8 pairs of cranial nerves out of the brainstem near the brainstem, and the compressor vessels It is often the anterior inferior cerebellar artery. (iii) Trigeminal nerve decompression is performed using an extra-superior cerebellar approach with a 1-cm wide cerebral pressure plate extended into the triangle composed of the cerebellum, cerebellar curtain and rocky crest, and the cerebellar wings are gently pulled apart and slowly penetrated deeper into the pontocerebellar paramedian area. Under the operating microscope, the arachnoid membrane over the rock vein is sharply cut, and the rock vein is mostly 2 to 3 branches from the cerebellar and brainstem surface veins converging into a trunk into the supratentorial sinus, which can be gently pulled in the posterior-superior direction to have enough clearance to penetrate deeper and complete the operation without cutting off the treatment. Sometimes, in order to expand the field space, bipolar electrocoagulation is used more than 2 times to confirm the occlusion of the vessel and then cut it. The clipping should be done against the cerebellar side to prevent pulling through the entrance bleeding. Protect the lateral facial nerve, further turn over the cerebellum, you can see the trigeminal nerve sensory root and its surrounding abnormal blood vessels deep above the facial nerve at 0.5 cm depth, identify the relationship between the nerve root and blood vessels and make decompression treatment.
Step 5: Nerve decompression: expose the area where the nerve is compressed by the vessel, probe the nerve travel area, and observe the anatomical relationship between the vessel and the nerve. The responsible vessel is identified. Since lateral position can cause displacement of the cerebellar artery, any vessel 1~2 mm from the nerve root is considered to be in contact with the nerve, especially if there are pressure marks on the nerve or if the nerve is pushed and twisted is reliable evidence. Nerve-vessel relationship and typing: The relationship between vessels and nerve roots are mostly horizontal and vertical crossings (more than 50%), oblique crossings or cross-wrap twists. In order to express this anatomical-pathological relationship of vascular cross-over and pulsation, it is divided into 4 types: contact, compression, adhesion encirclement and penetration, and the typing criteria are: ① contact type, vascular and nerve contact, no vascular indentation on the nerve root; ② compression type, vascular compression of the nerve, vascular indentation on the nerve root; ③ adhesion encirclement type, vascular cross-over and encirclement of the nerve root by the arachnoid or adhesion together, with nerve root deformation and displacement (iv) penetrating type, in which the vessel penetrates and compresses the nerve root. Decompression requires sharp separation of the artery from the arachnoid membrane and its adhesions around the nerve, and from the origin to the distal end.
The responsible vessel is freed with a long-handled microdebrider and pushed away from the nerve out of the brainstem, and a small piece of gelatin sponge is placed in front of the nerve. The responsible vessel is dislodged and pushed away from the nerve out of the brainstem toward the skull base. Generally, the vessel should be separated from the nerve gap as large as possible, leaving the brainstem from the nerve root to the dura mater more than 0.5 cm, and a square block of 1.0×0.5 cm can be placed between the two with a Tefflon cotton pad of appropriate size placed between the responsible vessel and the brainstem nerve root. Alternatively, the nerve bundle is incised longitudinally along the long axis of the nerve and separated, and the penetrating vessel is pushed to the dural side away from the nerve migration area and the spacer is placed. Tefflon cotton is placed by trimming the ends of the cotton at an acute angle with scissors and placing it in a flocculated, oval shape between the responsible vessel and the brainstem and posteriorly around the nerve. The anterior inferior cerebellar artery penetrating the seventh and eighth cranial nerves is likely to have branches innervating the pontine brain, and such penetrating branches must be preserved. Care should be taken to avoid placing the pad between the responsible vessel and the facial nerve, and not to contact the facial nerve at the exit of the brainstem to prevent local adhesions that could lead to postoperative recurrence. The pad should not be too large to avoid new compression and should be secured after placement to prevent slippage. After the responsible vessel is padded, the artery should not be twisted into an angle, otherwise it may affect the blood supply to the brainstem. When the responsible vessel is a thick, tortuous, sclerotic vertebral artery or the responsible vessel sends out several short and small penetrating arteries, penetrating between the brainstem and the facial and auditory nerves, the suspension method is used, that is, the pad cotton is made into a band around the vessel and then fixed on the rock dura with medical adhesive, which can improve the decompression effect of the facial nerve out of the brainstem and can avoid the injury of the small penetrating arteries.
Step 6: Cranial closure: After surgery, the pressure neck test confirms no bleeding, gentle flushing with warm saline, nimodipine warm saline or poppy base warm saline, bone wax sealing of the air space, and tight suturing of the muscles and fascia to avoid cerebrospinal fluid leakage.
In general, microvascular decompression is a craniotomy to reveal and dissect out the nerve in question and find the compressing vessels. A foreign body material is used to isolate and push away the responsible blood vessel that is compressing the nerve root, while completely preserving the normal function of the nerve and blood vessel. This material will not interfere with the nerve root and will not be absorbed. Once the responsible vessels are isolated, the source of irritation disappears and the hyperexcitability of the nerve nuclei disappears and normalcy is restored. The surgery is performed in a narrow space between the brainstem, cerebellum, and cranial wall, and there is no damage to brain tissue, nerves, or blood vessels, making the surgery safer. The vast majority of patients’ symptoms disappear immediately after surgery, and normal facial sensation and function are preserved without affecting the quality of life. The surgery requires only a partial shaving of the hair behind the ear and a small bone window, and the stitches are usually removed one week after surgery and the patient can go home. Since the skin incision is hidden in the hairline behind the occipital area, the scar is not easily visible and does not affect the aesthetics. Since microvascular decompression has the advantages of radical treatment, minimally invasive, low complications and extremely low recurrence rate, it is currently the safest, most effective, ideal and preferred surgical method for the treatment of cranial nerve diseases internationally recognized.
IV. Overall efficacy of MVD surgery
The efficacy of surgery depends on the accurate determination of the responsible vessel and the adequate decompression of the nerve root.
In 1992, Jannetta reported 366 patients who underwent surgery, and the results were 215 (58%) complete remission, 141 (39%) partial remission, and 10 (3%) no remission. worsened, and the success rate rose to 92.3% after 6 months, with 7.7% still having spasticity symptoms. The overall cure rate worldwide is between 82% and 99%, and the recurrence rate is only about 1-5%. Theoretically, the cure rate of this procedure should be close to 100%, and the main reason for this difference in efficacy is the experience of the operator, whose inexperience may result in the omission of the responsible vessel, incorrect placement of the pad into the Teflon cotton leading to inadequate decompression; secondly, because the vessel compressing the facial nerve root is too thick, it is difficult to perform effective decompression with the current decompression method, etc.
Patel A et al [28] completed MVD in 217 patients with GPN, 67% of the patients immediately achieved success, 25% improved, and 8% still had episodes. There are many similar reports, and it can be seen that the short-term efficacy after MVD is still very good.
2. Long-term postoperative follow-up: Jannetta 1990 reported 334 patients with 12-189 months follow-up (mean 68 months), 89% had complete remission, 5% had partial remission, and only 6% were ineffective, of which 10% were reoperated. Patel A was followed for 12-384 months (mean 68 months) and the results were 64% complete remission, 26% partial remission, and 10% failure, they also observed that all patients with typical GPN achieved remission. They also observed that all patients with typical GPN achieved remission. 62 cases of TN due to venous compression were followed up for more than 5 years after surgery, none of them recurred, 6 cases did not disappear completely after surgery but only reduced significantly, 2 cases were cured by gradual disappearance of pain after 2 and 1.5 years, and the other 4 cases required a small amount of carbamazepine but could be controlled. Tyler-Kabara EC et al. showed that in 969 cases of typical TN and 672 cases of atypical TN were followed up for 5 years after surgery. 80% of typical TN were significantly improved, while only 51% of atypical TN were improved. they concluded that the long-term efficacy of MVD in treating typical TN was significantly better than that of atypical TN. there are many other similar reports from home and abroad that the long-term effect of MVD is also good.
3. Reasons for ineffective microvascular decompression.
①Vessel leakage. The causes of vessel omission were considered to be possibly the intraoperative change of patient’s head position, cerebellar hemisphere pulling, too rapid cerebrospinal fluid discharge and extensive arachnoid dissection resulting in displacement of the responsible vessel stroke causing identification difficulties; secondly, the vessels parallel to or simply in contact with the nerve were mistaken for the responsible vessels and decompressed, and the main responsible vessels located deep in the vascular plexus were omitted.
②The isolation tampon slipped and displaced The isolation tampon used for the first MVD was small or improperly placed, and although the compression point was separated from the responsible vessel at that time, the isolation tampon slipped away from the decompression position with postoperative cerebellar repositioning and cerebrospinal fluid flow.
(iii) Too large or too many isolation tampons may cause the neuraxis to bend, displace, or form new pressure points. If the responsible vessel is tortuous, sclerotic or a short artery, the cotton sheet should be wrapped around the vessel and then fixed to the rocky dura to achieve adequate decompression
④Arachnoid adhesions are seen with extensive arachnoid adhesions, and re-performing vascular-neural relaxation has a clear therapeutic effect suggesting that the adhesions and thickened arachnoid may be the cause of new compressions.
⑤ Venous compression and other causes intraoperatively, three cases were found to have good placement of isolation tamponade for the first operation and disappearance of symptoms after re-MVD, the cause of which was not clear.
4. Prevention and control of complications: The main common complications in decompression surgery are cerebellar injury, hearing loss, facial hypesthesia and cerebrospinal fluid leakage; the rare ones are facial muscle weakness or paralysis, low group cranial nerve symptoms, and recurrence. There are also problems with intracranial hemorrhage, edema, and infection. With the exception of hearing impairment, which is more difficult to recover from (incidence around 2% to 5%), most cranial nerve injuries have mild symptoms and are mostly recoverable gradually, with serious complications less than 1/1000. the incidence of complications is closely related to surgical improvement and surgical technique. Cerebellar injury has decreased in the last decade, and the manifestations of the injury are both hemorrhage and contusion, and the cause of the injury is directly related to the force and duration of pulling the cerebellum. The prevention is to ensure that the posterior mastoid bone window adequately exposes the beginning of the sigmoid sinus and that the dural incision is close to the sigmoid sinus rather than posterior, both of which facilitate narrowing of the operative field while helping the operator’s line of sight to penetrate deeper along the rocky-inferior temporal bone margin without excessive retraction of the cerebellum. Cerebrospinal fluid leaks are most often caused by opening the mastoid ventricles and excursions away from multiple folded tissue layers. In addition to tight suturing of the dura mater, pressure on the cervical vessels and elevation of cerebral pressure to prevent leakage, attention should be paid to the alignment of the severed levels of the collar and neck, so that the four layers of sutures, deep muscle layer tendon membrane and capillary tendon membrane are intermittently sutured with intestinal thread to ensure that the capillary tendon membrane covers the full length of the incision and cerebrospinal fluid cannot leaking out. Postoperative cerebrospinal fluid leakage can be cured by lumbar puncture and drainage, with a few re-surgical sutures for dura and mastoid air chamber bone wax caulking.