Trigeminal neuralgia (sometimes called “face pain”) was first reported by Nicolas Andri in 1756 and is the most common type of facial neuralgia. It is a recurrent, transient, paroxysmal, severe pain confined to the area of the facial trigeminal nerve. The main feature is the sudden onset of pain without any aura, mostly on one side. The pain is as severe as a cut, electric shock, or lightning-like pain lasting from a few seconds to 1-2 minutes. It is often accompanied by lacrimation, drooling, flushing, and conjunctival congestion. The painful episodes are as normal as the remission period, often with trigger points, and the duration of the disease is usually long, without positive neurological signs.
The incidence of this disease is about 182/100,000 people. The disease is more common in middle age and old age, and the disease begins in those over 50 years of age. It is slightly more common in women than men, and most of the pain is unilateral, with the right side being the most common, and the incidence of bilateral pain is about 5%. It can be divided into primary and secondary.
Primary trigeminal neuralgia usually refers to those who do not show positive neurological signs, and its etiology is not completely understood so far. It is presumed that demyelination of trigeminal neuralgia is the main cause of trigeminal neuralgia, while mechanical compression, ischemia, and disorders of myelin nutrient metabolism may be the triggering factors of myelin loss.
Dever et al. further proposed the ignition hypothesis, suggesting that there are abundant ectopic excitatory sites in or near the demyelinated spots of trigeminal neuralgia patients, distal ends of severed axons and axonalized cells of sensory ganglia. There are abundant numbers of ectopic excitatory sites that are in a low-threshold, excitable state and can generate impulses autonomously or in response to subtle, non-injurious stimuli, while other sites are resting but have a microsensory threshold that triggers a spontaneous ignition process lasting tens of seconds in response to momentary stimulation, called post-release.
And this process is enhanced by the positive feedback effect between neurons. Pseudosynaptic crosstalk between neurons, where currents excite adjacent neurons directly from one neuron and interactively post-release afferent impulses evoked by nonsynaptic release of neurotransmitters or to interstitial excitation of neighboring neurons, causes synchronized post-release of sensory nerve fibers so that injurious impulses are amplified thereby triggering a burst of depolarization process.
Haines et al. conducted a more in-depth anatomical study of the relationship between the trigeminal nerve and microvessels and found that trigeminal neuralgia was present in 92.5% of cases of trigeminal nerve root compression in the presence of tiny paramedian vessels.
Janett (1981) suggested that the most common cause was vascular (mostly superior cerebellar artery) coiling around its unmyelinated trigeminal nerve root initiation, and that manifest microvascular decompression could terminate trigeminal neuralgia episodes, with venous compression seen in a few cases.
The causes of secondary trigeminal neuralgia have been identified as: pontocerebellar horn tumors (cholesteatoma, meningioma, auditory neuroma), trigeminal neurofibroma, nasopharyngeal carcinoma, cerebral arachnoiditis, and multiple sclerosis.
For secondary trigeminal neuralgia, treatment should be directed at the cause, for example, trigeminal neuralgia caused by tumor should be surgically removed, for primary trigeminal neuralgia, medication should be the first priority, if medication is ineffective or the side effects of medication are too great to continue taking medication, surgery can be considered.
Common vessels responsible for compression of trigeminal nerve
The vessels that compress the trigeminal nerve to produce pain are called “responsible vessels”. The common responsible vessels are: ① superior cerebellar artery (55%), the superior cerebellar artery can form a vascular loop that extends caudally and contacts the trigeminal nerve into the brainstem, mainly compressing the nerve root above or above the medial side. (ii) Anterior inferior cerebellar artery (30%), generally the anterior inferior cerebellar artery compresses the trigeminal nerve from below, and may also form a clamping compression on the trigeminal nerve together with the superior cerebellar artery. ③Basilar artery, with age and hemodynamic effects, the basilar artery may bend to both sides and compress the trigeminal nerve root, generally more bent to the side of the thinner vertebral artery. Other rare responsible vessels include the posterior inferior cerebellar artery, variant vessels (such as the permanent trigeminal artery), the transverse cerebral pontine vein, the lateral veins, and the basilar plexus. The responsible vessel can be one or multiple, and can be either an artery or a vein.
All responsible vessels that may produce compression (which may be one or more, in patients with lower trigeminal neuralgia pain, are due to compression of the superior anterior or posterior trigeminal nerve root by the superior cerebellar artery; while in those with upper pain, the nerve root is externally compressed by the anterior inferior cerebellar artery. The superior cerebellar artery and its branches (in the case of compression by the rock vein, the rock vein must be dissected) and the arachnoid cords are commonly “slackened”.
Sometimes, because the VA is thick and sclerotic, it is an indirectly responsible vessel, which may push the AICA or PICA and other directly responsible vessels together to compress the nerve, so it is often impossible to obtain satisfactory decompression effect by simply decompressing the facial nerve. Sindou et al. also pointed out that the spacer should be placed far from the root of the trigeminal nerve to achieve real decompression in order to obtain good long-term results. Long-term outcome. The gradual placement of Teflon wadding from the posterior group of cranial nerves from the bottom up to lift the VA is in line with the principle of complete decompression.
It has been reported that intraoperative application of nerve pulling hooks outside the nerve sheath and repeated combing of the nerve in the direction of the nerve can achieve the purpose of changing the abnormal pathological environment inside the nerve with good efficacy. Indications for partial trigeminal sensory root dissection: (1) multiple sclerotic plaque compression; (2) too tight adhesion of the vessel to the nerve root; (3) the artery branch supplying the pontine brain must be sacrificed to free the artery; (4) pontine intrinsic vein compression; (5) no definite cause of compression is found.
Indications for surgery
(1) manifestation of typical trigeminal neuralgia with the presence of “trigger points”; (2) exclusion of multiple sclerosis and CPA tumors; (3) drug tolerance, toxic side effects, and poor efficacy; (4) no serious organic disease and able to tolerate surgery; (5) facial numbness after other treatments cannot be accepted; (6) preoperative cranial MR (3D- SPGR) examination suggested a close relationship between the trigeminal nerve root and the adjacent peripheral vessels; (7) the patient’s choice of surgical intention.
Case
The patient was a female, 42 years old. She had been suffering from left trigeminal neuralgia for 4 years and had been taking carbamazepine for years, with teeth grinding (both day and night). “Microvascular decompression” was a miracle, and the pain and grinding symptoms disappeared, and the patient was completely free from trigeminal neuralgia.
Microvascular decompression is a widely used treatment for trigeminal neuralgia that is highly recommended by most scholars at home and abroad, because it is the only treatment for trigeminal neuralgia that targets the “cause”. Compared with other treatments, its biggest advantage is that it can preserve the anatomical integrity of the trigeminal nerve, release local vascular compression, and preserve the integrity of trigeminal sensory transmission without loss of facial sensation on the basis of long-term effective pain resolution. It can change the discomfort of facial numbness after the previous treatment, less permanent neurological dysfunction remains, improve the quality of life of patients, and make the majority of patients willing to accept the treatment. Some patients can also eliminate the state of hypertension caused by vascular compression of the brainstem after surgery, and achieve the purpose of eradicating hypertension. mvd surgery has good therapeutic effects, but also has certain risks, so choose a regular and guaranteed hospital for treatment.