Etiology of trigeminal neuralgia
1. The central etiology of trigeminal neuralgia paroxysms suggests a sensory epileptiform discharge, the site of which may be within the nucleus of the trigeminal spinal tract or elsewhere in the center. The sudden onset of trigeminal neuralgia, its short duration, the presence of trigger points, the effectiveness of antiepileptic treatment, and the focal epileptiform discharges recorded at the midbrain during painful episodes all support the central etiology theory. However, this theory is difficult to explain many of the phenomena seen clinically.
2. Peripheral etiology, i.e., the etiology is in the posterior root portion between the hemimelia and the pontine brain, is mostly reported in the literature as a peripheral lesion, with the following theories.
(1) mechanical compression or pulling of the trigeminal nerve root, mainly the adjacent blood vessels compress the trigeminal nerve root.
(ii) arteriosclerosis causes inadequate blood supply to the trigeminal nerve
③Multiple sclerosis or spontaneous demyelinating disease.
④Familial trigeminal neuralgia.
Most clinical data indicate that vascular compression of the trigeminal nerve root is the main cause of primary trigeminal neuralgia.
Hazards of trigeminal neuralgia
1. The harm of prolonged trigeminal neuralgia can cause a series of changes in the physiological activities of the circulatory system, neuroendocrine, respiratory system and digestive system.
2, Trigeminal neuralgia causes increased activity of sympathetic nervous system, which causes peripheral vasoconstriction, increased blood pressure and accelerated heart rate.
3. Patients with trigeminal neuralgia are often anxious and easily irritable, and many patients’ mental activities are in a state of inhibition, pessimistic and disappointed, unable to endure their pain, and even generating thoughts of lightness of life. Long-term depression will make the patient’s expression indifferent and unresponsive to external changes.
The attack characteristics of trigeminal neuralgia.
1. There is often no warning before the onset of pain, it is a sudden lightning, brief and intense pain, and each attack lasts from a few seconds to one or two minutes and stops abruptly.
2, the nature of trigeminal neuralgia pain is varied, it can be tear-like, electric burning-like, knife-like or needle-like, etc., which makes patients feel painful.
3.Patients have touch points, touching a part of the face can induce pain, mostly in the side of the nose, upper lip and teeth, etc. A touch can cause pain, so that patients dare not wash their faces, brush their teeth, get haircuts, eat and talk, etc.
4. Painful twitching: reflex twitching of facial muscles, with the corners of the mouth drawn to one side.
5. Accompanying symptoms: facial flushing, increased skin temperature, conjunctival congestion, lacrimation, increased saliva secretion, nasal mucosa congestion, and runny nose.
Differential diagnosis
1.Glottopharyngeal neuralgia
Location: one side of the tongue root, soft palate, tonsils, pharynx, deep part of the ear canal.
2.Pterygopalatine neuralgia (Sluder’s neuralgia)
The pain starts from the nasal root and is mainly distributed in the lower half of the face, producing discomfort in the eyes, nose, upper teeth, cheek, palate, and pharynx, and may also extend to the neck, shoulders, and upper extremities without trigger points.
3.Trigeminal neuritis
It can be caused by cold, inflammation of adjacent tissues, diabetes, poisoning, etc.
The pain is persistent and sometimes accompanied by motor branch dysfunction.
4.Atypical facial pain
It is difficult to determine the exact location, and the nature of the pain is “numbness”, “burning pain” and “ankylosis”, which is often beyond the distribution of the trigeminal nerve and is not triggered by slight touch.
The pain is persistent and may fluctuate in intensity, but there are rarely intermittent periods.
It is mostly seen in women of younger age.
5.Other: toothache, post-herpetic neuralgia, secondary trigeminal neuralgia
Anatomy of the intracranial segment of the trigeminal nerve
It is emitted from the base of the pontine brain and the pontine arm, and travels obliquely upward to the tip of the rock, which is surrounded by the Meckel cavity formed by the dura mater, and thus enters the middle cranial fossa, where the trigeminal nerve pressure marks are formed on the surface of the rock bone.
The position of the branches: the third branch of the sensory root is located inferiorly and laterally, the first branch is located superiorly and medially, while the second branch is located between the two, with many anastomoses between the three branches. The motor root is located medial-superior to the first branch.
The trigeminal sensory root has an elliptical profile, with the angle between the long axis of the ellipse and the long axis of the body ranging from 10 to 80°, mostly between 40 and 50°.
There are about 15 small nerve roots (motor or abberant sensory rootlets) at the entry of the trigeminal nerve into the pontocerebellum. Sometimes it is not easy to identify the sensory and motor roots clearly intraoperatively, and the sensory roots enter the three branches of the trigeminal nerve according to the position of the three branches.
In many cases, the formation of a localized labyrinthine process in the cerebellum interferes with the visualization of the root entry zone (REZ) of the trigeminal nerve.
Principles of trigeminal neuralgia treatment
Pharmacological treatment is preferred for the initial onset, and surgical treatment is considered when conservative treatment is ineffective.
Common responsible vessels
(1) Superior cerebellar artery (55%). The superior cerebellar artery may form a vascular loop that extends caudally and contacts the root of the trigeminal nerve, mainly compressing the nerve root superiorly or superiorly and medially.
(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.
The basilar artery may bend to the sides and compress the trigeminal nerve root with age and hemodynamic effects.
④Other 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.
Trigeminal nerve microvascular decompression
Rationale: Trigeminal neuralgia is caused by pulsatile compression of the sensory roots into the brainstem segment.
The REZ is particularly sensitive to pulsatile and cross-vessel compression, while peripheral nerves outside this segment are less susceptible to microvascular compression pain because they are wrapped by neurohypophyseal cells. In the elderly, due to arterial displacement or lengthening caused by atherosclerosis, vascular compression of the REZ zone, which is the termination of Schwann cells of the trigeminal nerve at the brainstem, forms an unmyelinated pocket of 0.5 to 25 px between the central and peripheral myelin sheaths and is only entrapped by oligodendrocytes. Compression of the microvasculature causes pseudosynapses to form between nerve fibers in the REZ, leading to short circuits in conduction.
Surgical procedure: The patient is placed in the lateral position, an arcuate incision of approximately 125px in length is made at the level of the external auditory canal, the occipital muscles are separated
The skull is exposed upward to above the transverse sinus and outward beyond the sigmoid sinus. The bones are drilled and a bone window is formed, within 2.5×62.5px in size; the dura is arched with the sigmoid sinus side as the base. The cerebral plate is retracted superiorly and laterally to the cerebellum, and the CPA pool is fully drained of fluid. The cerebellum was explored along the lateral aspect of the cerebellum toward the deep side, and the arachnoid was sharply separated, carefully protecting the facial auditory nerve and preserving the rock vein as much as possible. Adjust the depth of the microscope, sharply separate the arachnoid, clearly expose the trigeminal REZ and its surrounding vessels, and carefully identify the responsible vessels (offending vessels), which are mostly arteries, most commonly SCA, followed by AICA, sometimes basilar artery, and even PICA; occasionally they are venous compressions, and the veins are most commonly branches of the rock vein. The arachnoid membrane between the nerve and the vessel is fully relaxed, and a Teflon pad of appropriate size is placed between them.
Surgical efficacy: early surgical results in patients with facial pain disappeared after awakening from anesthesia, and most reported recent
The effectiveness rate is 82-95%. Approximately 40% of patients still have varying degrees of pain for several weeks after surgery, with relief within 2 to 8 weeks.
Postoperative recurrence: between 3 and 10%, with postoperative recurrence occurring mostly within the first 1 to 2 years after surgery and 5 years after surgery
The recurrence rate is less than 2% at 5 years after surgery, and less than 1% at 10 years after surgery.
Factors affecting recurrence: Trigeminal nerve REZ with arterial compression is less likely to recur, and intraoperative arterial compression or compression of blood vessels is not found.
The recurrence rate after surgery is high for those with arterial compression or venous compression. Patients with a history of less than 7 years have a good surgical outcome, while those with a history of more than 7 years are prone to recurrence. Women are prone to recurrence. Multi-branch involvement is less effective than single involvement, but is not related to lateralization. Previous history of trigeminal nerve surgery is also an influential factor in the long-term outcome. Those who have undergone radiofrequency thermal coagulation of trigeminal nerve, trigeminal nerve rhizotomy or with sensory impairment have poor results.