The authors treated a total of 1476 patients with trigeminal neuralgia using microvascular decompression (MVD) since 1986. Based on the anatomical observations of this group under the surgical microscope and combined with the literature, the causative factors of trigeminal neuralgia were analyzed, and the results are reported below.
Materials and methods
1. General data: Of the 1476 cases in this group, 887 were cases in 210 Hospital of the Chinese People’s Liberation Army (Duan Yunping was the director of neurosurgery in 210 Hospital), including 782 women and 694 men; age 43-85 years, average 61 years; duration of disease 1-18 years. The pain was located on the left side in 687 cases and on the right side in 789 cases; the first branch of the trigeminal nerve was involved in 20.5% (302 cases), the second branch in 60.7% (896 cases), and the third branch in 41% (605 cases). All cases were excluded by CT examination, 25 cases were examined by MRI, and 17 cases were found to have arterial compression of the trigeminal nerve. The 1476 cases in this group did not include 87 cases of trigeminal neuralgia caused by tumors in the pontocerebellar horn of the cerebellum.
2.Surgical method: All cases were treated with local anesthesia and small postauricular incision with a bone window of 1.5 cm. This approach could obtain a full view of the trigeminal nerve from the nerve root out of the pontocerebellum to the Michael’s bursa.
3. Anatomical observations focus on.
(1) The presence or absence of vascular compression and the degree of compression;
(2) The location of vascular compression and its relationship with the nerve;
(3) The presence of arachnoid adhesions between the nerve and the surrounding structures;
(4) whether there was atrophy of the nerve.
Results
1. The pathogenic factors of trigeminal neuralgia were divided into type III: type I: vascular compression with arachnoid adhesions 1363 cases, accounting for 93%; type II: pure vascular compression without arachnoid adhesions 110 cases, accounting for 7%; type III: no vascular compression and arachnoid adhesions 3 cases. The overall atrophy of the trigeminal nerve root could be seen, with atrophy to 1/3 of normal.
2. Different types of vascular compression and the degree of compression: only 3 cases without vascular compression were found in 1476 patients, and the remaining 1473 cases had one or more vessels compressing the trigeminal nerve. The superior cerebellar artery (alone or combined with other vessels) was compressed in 85% (1254 cases) of all patients; the anterior inferior cerebellar artery in 25.6% (376 cases); venous compression in 15.5% (229 cases); basilar artery in 3.3% (49 cases); and small unnamed artery or vein in 1.4% (20 cases). Among the 1473 patients with vascular compression, 1105 cases (75%) of the responsible vessels contacted the nerve root, but there was no obvious indentation on the nerve root; 368 cases (25%) had obvious indentation on the nerve root.
3, trigeminal nerve root arachnoid adhesions: 1363 cases (93%) in this group could be found to have locally thickened arachnoid adhesions with the nerve. There are two most common types. type I: trigeminal nerve root in situ adhesions, trigeminal nerve travels normally, but there are arachnoid adhesions causing nerve root fixation, type I accounts for 28% (382 cases). type 11: trigeminal nerve root ectopic adhesions, nerve root displacement, distortion, and arachnoid adhesions making it fixed, type II is common, accounting for 72% (981 cases).
4. Site of compression along the nerve root: Among the 1473 patients with vascular compression, 481 cases (32.6%) had more than two vessels compressed, but one vessel was found to be the responsible vessel intraoperatively. The responsible vessel compression site was in the area of the nerve root into the brainstem in 46.9%, in the middle of the nerve in 44.7%, and near the bursa of Michael in 8.4%.
DISCUSSION
In the pathology of trigeminal neuralgia, vascular compression of the nerve plays a crucial role, which has been confirmed by a large number of cases¨ . Under normal circumstances, the trigeminal nerve is in a collateral relationship with the adjacent blood vessels, which are often in contact with each other, but the trigeminal nerve is immobile, in a “floating” state, and no compressive force is generated between the nerve and the vessels. showed that 29 of the 50 trigeminal nerves were in contact with adjacent arteries. The authors had a group of 387 patients with facial spasm who were found at surgery to have 27% of the superior cerebellar artery or anterior inferior cerebellar artery in contact with the trigeminal nerve, but none had a history of pain. Only 3 cases in this group had no vascular compression, and only nerve root atrophy was found to 1/3 of its original size; while vascular compression was found in the remaining 1473 cases. 1363 cases (93%) were found to have varying degrees of arachnoid adhesions, which immobilized the trigeminal nerve, thus causing the normal vascular-neural contact to be transformed into a permanent and constant compression due to the immobilization of the trigeminal nerve. Yunping Duan has proposed that “arachnoid adhesions are the etiological basis of trigeminal neuralgia”. In our group, only 110 cases (7.0%) had simple vascular compression without arachnoid adhesions, which was due to congenital compression by overgrown vessels or arteriosclerosis. The authors concluded that the occurrence of vascular to nerve compression was due to congenital vascular overgrowth or atherosclerotic compression, and more importantly, due to trigeminal nerve fixation caused by arachnoid adhesions, which transformed the normal contact between nerve and vessel into compression. In our group, 93% of the patients were accompanied by arachnoid adhesions. Except for some of the patients who underwent secondary surgery in which the cause of arachnoid adhesions could be determined, other cases were due to compression irritation, inflammatory reaction, or other factors causing arachnoid adhesions, which cannot be determined based on current experience and need to be further studied.
In the early days of MVD, it was thought that the trigeminal nerve enters the brainstem area (REZ) 2-3 mm as a zone of absence of myelin, which can cause painful attacks when compressed by blood vessels. Later surgery revealed that vascular compression could exist in all areas from the Michael’s bursa to the entry brainstem. There was electron microscopic ultrastructural confirmation that regional demyelination changes were seen in the compressed nerve roots of trigeminal neuralgia, and this change affected the impulse afferent function of trigeminal nerve fibers, causing subthreshold excitation of the sensory nucleus of the trigeminal nerve, which decreased the sensory stimulation threshold of nerve endings and put them in a state of hypersensitivity. In this group, the site of vascular compression was 46.9% in the REZ, 44.7% in the middle of the nerve root, and 8.4% in the vicinity of the Michael’s bursa, confirming the presence of vascular compression in the whole segment of the nerve root. In addition, vascular compression away from the REZ, for example, when an overgrown superior cerebellar artery pushes down on the middle third of the nerve root, often produces a pull on the REZ in addition to the compression, which is also an important cause of pain. Therefore, when performing MVD surgery, the entire trigeminal nerve from the Michael’s bursa to the cerebral bridge should be examined. When vascular compression is found, nerve root adhesions must be noted. If there are adhesions, it is important to achieve a full release of the nerve, which will facilitate the implantation of the spacer and will avoid angulation of the vessel after the spacer. After finding the responsible vessel for compression, it should also be checked for other vascular compressions. 32.6% (481 cases) of this group had multiple vascular compressions. Treatment of one compressed vessel alone often leads to poor postoperative results or recurrence of pain after a period of time.
Reports on the negative rate of intraoperative vascular compression vary. In the 1980s, the percentage of patients without vascular compression was reported to be 18%-28.5%; whereas in 1996, Barker et al. reported that vascular compression was found in 1204 patients, 132 of whom had unrelieved pain after the first surgery and were confirmed to have vascular compression by reoperation. The negative rate of vascular compression in this group of cases was 3/1476. The authors concluded that the reasons for the high negative rate were.
(1) Failure to examine the trigeminal nerve root throughout;
(2) Ectopic adhesions occurred in the trigeminal nerve and the compression vessels were located at the base of the trigeminal nerve;
(3) Missing small unnamed vessel compressions. The surgeon’s experience can reduce the number of negative exploration findings by a considerable amount.