The use of percutaneous trigeminal nerve balloon compression for trigeminal neuralgia was a technique created by Mullan in 1978 and published by Mullan and lichtor in 1983. Background In 1952, Taarnhoj reported a group of patients who were treated for trigeminal neuralgia using posterior root decompression rather than dissection; until then trigeminal neuralgia had been treated using conventional dissection. 1955, Shelden et al. reviewed the advantages of decompression of the II-III branches of the trigeminal nerve and found that their own observations and Taarnhoj’s results had something in common; both groups of patients had pain relief Shelden concluded that there was a mild trauma to the menisci that was not conscious in both groups, and thereafter, Shelden treated only with compression intraoperatively. 1959 Svien and Love noted that in 91 patients treated with the Tanrnhoj method, with a 5-year follow-up, 85% of patients without subjective or objective sensory loss had recurrence of pain, and only In 1963 Graf reviewed a group of 100 patients treated with the Shelden method, also observed for about 5 years, and confirmed the same results, with a recurrence rate of 24%. Based on this information, Mullan created the percutaneous trigeminal nerve balloon compression, after he had already created the percutaneous spinal cord dissection. Mullan’s initial rationale for this procedure was that it was technically simple, less time-consuming than the most commonly used radiofrequency electrocoagulation dissection of the trigeminal meniscus, and did not require the patient’s awake cooperation, which was a fundamental advantage. Subsequent studies have found that this method has some other advantages, as well as other percutaneous puncture procedures, avoiding the complications of craniotomy, which can be disabling and fatal, although few; unlike other percutaneous puncture procedures, the puncture guide needle does not enter the foramen ovale, thus avoiding complications caused by accidental puncture of intracranial structures; this method also does not cause loss of corneal sensation, avoiding keratitis complications; and finally. Because the procedure is done under general anesthesia, the pain and stress inherent in other percutaneous puncture procedures are eliminated; the difference can be felt by any patient who has undergone other percutaneous puncture procedures and this procedure. Complications: 1. The autonomic reflex effect pain reflex has been well studied and can be completely blocked by preoperative administration of atropine if its presence is not wanted. If atropine (which can cause tachycardia) is not desired, a non-placement pacemaker, set to start pacing at a heart rate of 45 beats per minute, can also be used. Cases of cardiac arrest for 15 seconds or longer have been reported in patients not protected by a pacemaker, for which recovery was achieved simply by immediate release of balloon compressions and administration of atropine. The heart rate usually begins to increase before atropine is able to act, but in any case atropine should always be available and used early when there are signs that the patient may have a particularly sensitive pain reflex (e.g., significant bradycardia when the needle reaches the foramen ovale or when the balloon is just starting to inject fluid). In sensitive patients, atropine should be used before the onset of bradycardia. 2. Ipsilateral bulbar conjunctival congestion immediately at the end of the sensory loss procedure, with or without tearing, is indicative of a good outcome. The patient is pain-free when awake, but there is discomfort at the puncture site, which is more pronounced if there is a hematoma. Because nociception is only decreased and not completely blocked, this pain or discomfort is to be expected. Tactile sensation and sensitivity to needling on the surgical side also decreased, with the third branch being the most pronounced, the second branch the second most pronounced, and the first branch the least pronounced. Although sensation is only slightly altered in the second branch and may not be altered in the first branch, pain in these areas may have disappeared completely. Some patients may have sensory hypersensitivity when first awake, which gradually turns into hypoesthesia later, but rarely there is a significant sensory deficit. Decreased itching on stimulation of the ipsilateral nostril predicts a good outcome. Corneal reflexes may be decreased or normal. Balloon compression differs from radiofrequency electrocoagulation in that damage to A-δ and C class fibers is relatively mild. To selectively preserve the fine myelinated and unmyelinated fibers, the corneal reflex is also selectively preserved, and transients are mediated by these fibers. In the days following surgery, some patients can develop orofacial herpes, especially those with previous herpes, which is usually a sign of adequate compression and good results. If the sensory deficit is not significant or is not present at all, it is likely that the pain will not be relieved or will recur early after surgery. Sometimes intraoperative compression is inadequate, but the patient can get pain relief with carbamazepine, whereas the same dose of carbamazepine before surgery is ineffective. Occasionally the pain persists until 1-2 days postoperatively and then resolves. This phenomenon has been seen after the Taarnho j/Shelden procedure (nerve root release), and Sweet has reported cases where radiofrequency electrocoagulation was abandoned midway through the procedure and no disfiguring lesion was made at all, but the patient still had a brief period of pain relief. Postoperatively, patients generally experience subjective facial numbness and discomfort, which is less pronounced after 3 to 4 weeks and is described by some patients as “like just putting on dentures or corneal contact lenses”. Patients with a tendency toward obsessive-compulsive behavior are easily disturbed by any imperfection. If this patient is noted preoperatively, the surgeon should inform him that microvascular decompression is an alternative treatment option to balloon compression, which is a nerve-destroying procedure. Subjective numbness and objective hyperalgesia (hypoesthesia tactile hypoesthesia and hypalgesia pain hypoesthesia) are more variable and usually more severe within 3 to 6 months. The gradual disappearance of hyperalgesia does not necessarily mean that pain recurs, nor does persistent hyperalgesia guarantee that pain will not recur. Pain relief generally lasts until after facial sensation has been restored, because good facial sensation does not require complete restoration of nerve integrity. In cases of recurrence after microvascular decompression, significant atrophy of the nerve can be found upon reoperation, but the patient’s facial sensation can be well preserved. 3. Masticatory weakness is seen in almost all patients after surgery with ipsilateral temporalis and occlusal muscle weakness, most of which recover within three months. Many patients do not realize that they are only chewing with the contralateral side for months or even years. Some patients, especially those with dentures, may feel a misalignment of the bite and individually feel abnormal movement of the temporomandibular joint (very rarely painful). This discomfort due to muscle strength imbalance can be treated with anti-inflammatory drugs until the muscle strength returns to normal. The incidence of abnormal sensation after balloon compression is reported to be 12%, including pins and needles, dripping sensation, ants walking sensation, tightness and mild burning sensation. When the burning sensation is intense and the abnormal sensation or hyperalgesia severely bothers the patient, the condition is referred to as painful dysesthesia. This condition is more prominent (about 4% to 5%) in the early developmental stages of this procedure, when balloon compression has to last for several minutes, or when the patient has received other destructive treatments such as alcohol injections, but has largely disappeared in recent patients. 5. The recurrence rate of trigeminal neuralgia 5 years after surgery is about 15-20%, and the Kaplan-Meier survival curve shows a steady, slow and continuous rise in the recurrence rate until the tenth year, reaching about 30%. If carbamazepine is ineffective, patients may opt to undergo balloon decompression again, or in the case of patients in good physical condition, microvascular decompression. Most patients choose to undergo balloon compression again, believing that they can tolerate the accompanying facial numbness. Reoperation does not cause additional technical difficulties. Patients with multiple sclerosis have a high relapse rate of up to 30%. These patients may require multiple surgeries during their lifetimes. We believe that even if the recurrence rate is a little higher, it is better not to have too much balloon compression in order to avoid the development of painful sensory abnormalities, for which such patients are at high risk. For patients with bilateral trigeminal neuralgia, if the strength of the masticatory muscles has been restored after balloon compression on one side, this procedure can be performed again on the opposite side. However, the patient may have difficulty chewing if the other side is numb and the other side is numb. We have had a case where one side had undergone a classical trigeminal nerve 2-3 branch dissection at the base of the middle cranial fossa (preserving the motor branch) and the oral side was completely numb. The opposite side had undergone another balloon compression and the patient had no problems. Usually, if the patient has significant postoperative numbness on one side, a significant microvascular decompression can be performed on the contralateral side as much as possible. Patients with multiple sclerosis are particularly prone to bilateral pain, and in our experience, these patients tolerate bilateral staged procedures well. Histologic studies on the nature of trigeminal nerve injury have shown that balloon compression selectively damages tactile medullary thick fibers and preserves nociceptive metamyelinated thin fibers, which is completely different from the selective damage known from thermal coagulation disruption. Balloon compression may have reduced the transmission of sensory impulses and turned off the trigger switch of the trigeminal pain transmission pathway. Other complications Since 1983, multiple groups of balloon compression cases have been reported worldwide, totaling more than 8,000 cases, and some of the following complications have been seen: one death. In this case, a sharp puncture guide needle was used and pierced the foramen ovale. Postoperative subarachnoid hemorrhage resulted in hydrocephalus, multiple shunt procedures, and later death due to infection. By using a blunt-tipped guide needle, such complications can now be ruled out. In another case, the catheter was reportedly inserted into the internal carotid artery (without complications), which is difficult to imagine if the guide needle had not been inserted into the internal carotid artery. One group of cases, in which a smaller size 3 Fogarty catheter was used, reported a higher rate of recurrence . Loss of corneal sensation occurs rarely, and this risk has been greatly reduced by the use of pressure controllers. Other researchers have reported balloon compression under local anesthesia, but this forgoes one of the major advantages of balloon compression, namely that the procedure is painless.15 Short-term abducens nerve weakness has also been observed. Two cases of postoperative arteriovenous fistulae, one in the dura and one in the pterygopalatine fossa, did not require surgical treatment as they were only occasionally murmurous. In another case, an arteriovenous fistula formed in the maxillary artery of the patient and caused a persistent murmur. These experiences suggest that the foramen ovale should not be punctured with a sharp guide needle. In conclusion, percutaneous trigeminal nerve balloon compression has been used for 20 years and has proven to be a very effective and safe surgical treatment for trigeminal neuralgia, with a recurrence rate roughly similar to that of radiofrequency electrocoagulation of the meniscus, glycerol injection of the meniscus, and microvascular decompression of the trigeminal nerve root. This technique is simpler than hemi-lunar radiofrequency coagulation and hemi-lunar glycerol injection, and the fact that it is performed under general anesthesia makes it painless for the patient a major advantage. This technique also allows some selection of the three sensory roots of the trigeminal nerve and is particularly suitable for patients with pain in the first branch, as balloon compression selectively preserves the unmyelinated fibers that conduct corneal sensation, which has less risk of causing loss of corneal reflexes (using pressure-controlled techniques). Unlike apparent microvascular decompression, balloon compression is not a cause-specific treatment, but this technique is less expensive, less invasive, and less painful for the patient. Because such patients can be very difficult to manage, these advantages in the choice of surgical treatment.