Microvascular decompression is the short name for one of two common neurosurgical procedures used to treat trigeminal neuralgia. The procedure is used when trigeminal neuralgia at the exit site of the nerve in the posterior fossa is caused by pathologic contact with the supplying artery. The procedure involves elimination of compression by insertion of tiny pads of muscle tissue or suitable plastic material.
What is microvascular decompression?
Jannetta’s microvascular decompression of the trigeminal nerve refers exclusively to a neurosurgical procedure to remove compression of the trigeminal nerve at its point of exit from the brain in the posterior fossa. The full name of the neurosurgical procedure is microvascular decompression of the trigeminal nerve according to Jannetta. The paired trigeminal nerve, also known as the facial nerve and the fifth cranial nerve, consists of sensory and motor fibers. The nerve divides into three branches, the ophthalmic, maxillary and mandibular branches, before exiting the brain. The nerve contains mainly sensory fibers, but also some motor fibers to supply the masticatory muscles. In the area where it exits the brain in the posterior fossa, chronic high blood pressure and excessively narrow microvascular arteries can cause damage to the myelin sheaths of certain nerve fibers due to their pulsatile pressure, resulting in a type of short circuit between the fibers, causing the extremely painful trigeminal neuralgia. Microvascular decompression is considered for individuals whose trigeminal neuralgia no longer responds to medication and the cause of the extremely painful neuralgia can clearly be identified as nerve compression.
Function, effect, and goals
Jannetta’s microvascular decompression of the trigeminal nerve refers exclusively to a neurosurgical procedure to remove compression of the trigeminal nerve in the area of its exit from the brain in the posterior fossa. Before the intervention, which goes back to Prof. Dr. Peter Joseph Jannetta, Siegen, Germany, and which he introduced in 1976, it must be established that the compression of the trigeminal nerve is caused by blood vessels and not by other circumstances such as inflammation or, for example, a tumor. In addition, it should be ensured that the symptoms cannot be cured or at least greatly alleviated by drug treatment. Diseases such as multiple sclerosis (M), meningitis and congenital anomalies such as syringobulbia and Chiari malformation are considered contraindications for such an intervention. Neuralgia, which manifests itself in sudden stabbing pains or spasms – usually lasting only a short time – can affect all areas of the face and neck that are innervated by one of the three nerve branches of the trigeminal nerve. Modern imaging techniques such as magnetic resonance imaging (MRI) and computed tomography (CT) are used to make a clear diagnosis. The goal of invasive microsurgical neurological intervention is to permanently correct the microvascular compression. In more than 70 percent of cases, trigeminal compression is caused by the superior cerebral artery. During the procedure, the surgeon places a tiny pad between the artery compressing the nerve and the trigeminal nerve to distribute the previously punctate pressure over a larger area. Teflon pads, gelatin sponges or, alternatively, autologous muscle tissue are used as the material to distribute the pressure at the compression site. As a rule, immediate and spontaneous improvement of symptoms occurs postoperatively after removal of microvascular compression. Often the symptoms decrease again in the period after the operation until they disappear completely. The medication can then be gradually reduced in dose and finally discontinued completely. The postoperative improvements indicate that damaged myelin sheaths of the nerves can regenerate to a certain degree after compression is removed. The chances of success of microvascular decompression are over 90 percent.The advantage of the procedure compared to the alternatively applied percutaneous thermocoagulation according to Sweet is the complete preservation of the functionality of the nerve fibers of the trigeminal nerve. The success rate of thermocoagulation is similar to that after a microsurgical intervention according to Jannetta. However, thermocoagulation specifically destroys nonmyelinated nerve fibers by applying precisely measured amounts of heat at 60 to 80 degrees Celsius. However, the procedure also has the advantage that it can be repeated without complications in the event of recurrence.
Risks, side effects, and hazards
Microvascular decompression records the best long-term success of all procedures for the treatment of trigeminal neuralgia. In addition, it is a nondestructive procedure because the functional capacity of the trigeminal nerve is preserved. Compared with percutaneous procedures performed under local anesthesia, microvascular decompression carries higher surgical risks. In addition to the higher general risks associated with surgical procedures performed under general anesthesia, there are also a few special risks. The special risks may be temporary or permanent. First, there is a small risk of temporary or permanent facial nerve palsy, which can manifest as partial unilateral paralysis of facial expression with loss of sensory function. Another risk, also low, is unilateral temporary or permanent hearing loss. The mortality risk is reported to be 0.5 to 1 percent. While there is a small, but still feared, risk of anesthesia dolorosa in the other procedures, this specific risk can be eliminated in microvascular decompression. Anesthesia dolorosa is manifested by persistent, extremely uncomfortable continuous pain with concomitant loss of surface sensitivity. There is a low risk with percutaneous procedures because, for example, thermocoagulation of the gasserian ganglion destroys nerve fibers and these symptoms occur predominantly in nerve lesions.
