Brainstem nuclei associated with the trigeminal nerve
Trigeminal spinal tract nucleus: receives somatosensory fibers from the trigeminal nerve and is associated with cephalofacial nociception and temperature perception.
Trigeminal pontine nucleus: receives somatosensory fibers from the trigeminal nerve and is associated with tactile pressure sensation in the head and face
Trigeminal motor nucleus: Emits fibers that form the motor roots of the trigeminal nerve and innervates the masticatory muscles.
Mesencephalic nucleus of the trigeminal nerve: associated with the proprioception of the masticatory muscles and the extraocular muscles of the facial nucleus.
Anatomy of the intracranial segment of the trigeminal nerve
Course: Emanates from the base of the pontine brain and the pontine arm, travels obliquely upward to the tip of the rock, is surrounded by the Meckel’s cavity formed by the dura, and thus enters the middle cranial fossa, where the surface of the rock bone forms the trigeminal nerve indentation.
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 exposure of the root entry zone (REZ) of the trigeminal nerve.
Branches of the trigeminal nerve
Ophthalmic nerve
It contains somatic afferent fibers and runs through the lateral wall of the cavernous sinus, beneath the accompanying motoneurone and talocrural nerves, to the supraorbital fissure where it divides into three branches that enter the orbit via the supraorbital fissure.
Lacrimal nerve: distributed in the lacrimal gland, upper lid and skin of the external canthus.
Frontal nerve: divides into the supraorbital and supraorbital nerves approximately in the middle of the orbit, distributing over the skin of the frontal apex, upper lid, medial canthus, and dorsum of the nose.
Nasociliary nerve: Emanates from the subglottis nerve, anterior septal nerve, posterior septal nerve, and long ciliary nerve, which are distributed to the eyeball, pterygoid sinus, septal sinus, lower lid, lacrimal sac, nasal mucosa, and skin of the nasal dorsum.
Branches of the trigeminal nerve
Maxillary nerve
Containing somatic afferent fibers, it travels through the lateral wall of the cavernous sinus, exits the skull along its lower part through the foramen ovale, enters the upper part of the pterygopalatine fossa, continues anteriorly through the infraorbital fissure into the orbit, and continues as the infraorbital nerve.
Infraorbital nerve: exits the orbit through the infraorbital sulcus and infraorbital canal, distributing over the skin and mucosa of the lower lid, nasal flank, and upper lip.
Zygomatic nerve: It divides in the pterygopalatine fossa and distributes in the skin of the zygomatic and temporal areas.
Superior alveolar nerve: divided into anterior, middle and posterior branches of the superior alveolar canal, distributed in the maxillary teeth, gums and mucosa of the maxillary sinus.
Pterygopalatine nerve: distributed in the palate, nasal mucosa and palatine tonsils.
Branches of the trigeminal nerve
Mandibular nerve.
The anterior trunk is small and sends out muscle branches to the masticatory muscles, tympanic tensor, palatal sail tensor, and also the buccal nerve. The posterior trunk is thick and distributes to the dura mater, mandibular teeth and gums, the mucosa of the anterior 2/3 of the tongue and the floor of the mouth, the auriculotemporal region and the skin below the oral fissure, and also sends out branches to innervate the mandibular hyoid muscle and the anterior belly of the bicuspid muscle.
Auriculotemporal nerve: distributed in the skin of the temporal region, with branches to the parotid gland, joined by branches of the glossopharyngeal nerve.
Buccal nerve: distributed in the skin of the buccal region and the mucosa of the lateral walls of the oral cavity.
Lingual nerve: distributed in the floor of the oral cavity and the mucosa of the anterior 2/3 of the tongue, joined by branches of the bulbar cord.
Inferior alveolar nerve: It is distributed in the mandibular teeth and gingiva, and the terminal branch comes out through the chin foramen, called chin nerve, which is distributed in the skin and mucosa of the chin and lower lip. Its motor fibers innervate the lingualis muscle and the anterior belly of the bicuspid muscle.
The masticatory nerve: including the occlusal nerve, the deep temporal nerve, the internal pterygoid nerve and the external pterygoid nerve, which innervate the four masticatory muscles respectively.
Anatomical relationship of the trigeminal nerve
Trigeminal nerve distribution area
Illustration
Overview
Features: recurrent episodes of sudden, transient, severe pain in the trigeminal nerve division.
Epidemiology: It is mainly seen in middle-aged and elderly people, with a peak incidence between 50 and 70 years old and a trend of increasing incidence with age. The annual incidence is about 3.4/100,000 in men and 5.9/100,000 in women, slightly more than in men.
Classification: primary and secondary, with the latter mostly due to tumors in the CPA area, arachnoiditis, vascular malformations, aneurysms, and multiple sclerosis.
Etiology
The etiology of primary trigeminal neuralgia is unclear. Several theories.
(1) Vascular compression theory.
(2) mechanical compression theory
(3) Ischemia theory
(4) Central pathogenesis theory
(5) Others:
Vascular compression theory
The most popular and accepted view by many scholars.
(1) Microvascular compression of nerve roots
In 1934, Dandy first proposed that compression of nerve roots by blood vessels was one of the causes of pain, but did not mention the issue of decompression.
In 1959, Gardner first reported one case of successful neurovascular decompression.
In 1967, Jannetta confirmed Dandy’s suggestion that vascular compression was the cause of trigeminal neuralgia and pioneered microvascular decompression.
In 1980, Jannetta found arterial, venous, or mixed arterial and venous compression of the trigeminal nerve in up to 95% of 411 trigeminal neuralgia procedures; Zorman reported 125 patients with trigeminal neuralgia and intraoperative vascular compression of the nerve root was seen in 90 (72%) cases. See Figure.
Overview of trigeminal neuralgia
②Internal carotid artery compression : Kerr proposed that the top of the bone of the internal carotid artery canal can often be absent replaced by fascial tissue, so the ventral root of the meniscus and its branches are in close contact with the internal carotid artery below, and the pulsation of the carotid artery causes the disintegration of the myelin sheath of the meniscus and posterior roots and causes pain.
Mechanical compression theory
Compression by the dural sheath or crest: The trigeminal ganglion and posterior roots are compressed by the dural sheath and supratrochlear sinus that encase it or by the angular distortion of the posterior roots at the elevated crest when they pass through the dural foramen. In 130 patients with trigeminal neuralgia, the height of the rock crest on both sides was examined and the incidence was 3 times higher on the side with a slightly higher rock crest.
Ischemia theory
Trigeminal neuralgia is caused by atherosclerosis and cerebral ischemia and hypoxia, and is recurrently caused by the blockage of blood circulation and the production of pain-causing substances.
Wilson (1954) suggested that the disease is a paroxysmal distribution of trigeminal neurons located in the center, similar to sensory epilepsy. It has been suggested that the site may be within the nucleus of the spinal tract of the trigeminal nerve.
Pathology
Loss of ganglion cells, demyelination/myelin thickening of nerve fibers, and thinning of axes.
Microvascular compression
Clinical manifestations
Pain characteristics.
Aura: most of the attacks are not preceded by aura, the pain comes suddenly by abruptly stopping, and there is no pain between attacks.
Nature: electric shock-like, lightning-like, knife-like; the face can be distorted or frozen when the pain attack is severe.
Duration: each attack usually does not exceed 2 minutes, but after the attack the patient may have a residual dull pain or burning sensation in the face.
Frequency: early episodes are less frequent and can occur once in a few days, later they are more gradually aggravated, even once in a few minutes. The course of the disease may be periodic, with a cycle of several weeks to several months.
Painful twitching: reflex twitching of facial muscles with the corners of the mouth drawn to the side.
Concomitant symptoms: facial flushing, increased skin temperature, conjunctival congestion, lacrimation, increased salivation, nasal mucosa congestion, and runny nose.
Clinical manifestations
Trigger point and triggering
Also known as trigger point (trigger point), it is often located somewhere in the distribution area of the trigeminal nerve on the diseased side, such as the upper and lower lips, nose, corner of the mouth, incisors, palate, and buccal mucosa.
The pain of the mandibular branch is mostly caused by jaw movements (chewing, talking, yawning), and direct stimulation of the skin trigger point induces pain is rare.
The maxillary branch, on the other hand, is mostly caused by stimulation of trigger points (outer 1/3 of the upper lip, upper incisors, cheek, and inner part of the eye), and can be caused by washing the face, brushing the teeth, shaving, and blowing the nose.
Pain sites.
Lateral: mostly limited to one side, slightly more on the right side, 4% of patients have bilateral pain, mostly seen in patients with multiple sclerosis.
Branches: The 2nd and 3rd branches are most commonly involved at the same time, followed by the 2nd and 3rd branches alone, and the ophthalmic branch is the least common.
Trigeminal neuralgia-trigger point
Trigeminal neuralgia-diagnosis
Unilateral facial episodes of transient and severe pain
Trigger point and painful twitching are often present
No positive signs on neurological examination
Trigeminal neuralgia-differential diagnosis
Secondary trigeminal neuralgia: can be due to multiple sclerosis, medullary cavitation, primary or metastatic skull base tumor. Trigeminal nerve palsy (facial hypesthesia, blunted corneal reflexes, etc.) with persistent pain, often combined with other cerebral nerve palsy;
Toothache: toothache is usually persistent and dull, confined to the gum area, and may be aggravated by eating cold or hot food.
Trigeminal neuralgia – differential diagnosis
Glosspharyngeal neuralgia: It is a severe pain located deep in the tonsils, tongue, pharynx, and ear canal. Swallowing, coughing. Speech can be triggered
Sinusitis: localized persistent dull pain, localized pressure, fever, runny nose, increased white blood cells and other inflammatory manifestations.
Trigeminal neuralgia – differential diagnosis
Atypical facial pain: The pain is variable in location, deep and diffuse. It is often bilateral and has no tenderness. It occurs in patients with depression, hypochondria and personality disorders.
Temporomandibular joint disease: mainly pain during mastication, localized pressure pain
Treatment of trigeminal neuralgia
Drug treatment: The first choice for trigeminal neuralgia is the application of antiepileptic drugs, most commonly carbamazepine, phenytoin sodium, etc.
Surgical treatment: including closure therapy, radiofrequency thermal coagulation therapy, stereotactic radiosurgery therapy, surgery and other methods.
Treatment principles of trigeminal neuralgia
Drug treatment is preferred for the initial onset.
Consider surgery when conservative treatment is ineffective.
MVD is preferred for those who are physically fit and the patient agrees.
For those who cannot tolerate open surgery, radiofrequency thermal coagulation or gamma knife treatment can be considered.
If the above treatment fails, MVD, radiofrequency thermal coagulation or γ-knife treatment can be considered again after MVD, and radiofrequency failure can be considered repeatedly.
Trigeminal neuralgia – treatment
Drugs for the purpose of pain relief.
Carbamazepine : 0.1 Bid onwards, increasing by 0.1 daily to a maximum dose of
1.0 g/d Effective maintenance dose 0.6-0.8 g/d
Phenytoin sodium: 0.1 Tid up to 0.05 daily
Maximum dose is 0.6 g/d
Clonidine: 0.5 mg Tid onwards, increasing by 0.5 mg daily
Gradual increase to 4~6 mg/d, half of the cases can be controlled
Pemethrin: 2mg Bid onwards, increase 2mg/d to 6mg Bid
Chlorpheniramine: (baclofen) 5mg Tid onwards
10mg Tid, can be increased to 60~80mg
Trigeminal neuralgia – Treatment
High dose of vitamin B12
1000~3000ug/dose intramuscular injection, 2~3 times a week, 4~8 weeks of treatment
The first dose of 1000ug, the second 2000ug, the third 3000ug, maintain until the effect of the treatment
Local injection can also be given according to nerve distribution
Trigeminal neuralgia – Treatment
Occlusion therapy
Transcutaneous semilunar node radiofrequency electrocoagulation
Surgical treatment: trigeminal nerve sensory root partial excision
Microvascular decompression
Surgical treatment of trigeminal neuralgia (according to the different parts of the trigeminal nerve conduction pathway)
Closure treatment
Theoretical basis: Drugs with destructive effects on nerve fibers are injected directly into the branches of the trigeminal nerve or the semilunar ganglion.
Indications: Those who are ineffective in drug treatment or have adverse reactions and refuse surgery or are not allowed to have surgery due to physical conditions.
Methods.
Peripheral branch closure: for infraorbital body meridian, supraorbital nerve, chin nerve, mandibular nerve, etc.
Trigeminal nerve hemimelia closure: must be performed under X-ray surveillance.
Effectiveness: peripheral branch closure is easy to accomplish, but the validity period is usually 1-6 months; hemianopia closure has long-lasting efficacy, but the injection technique is difficult. Literature reports: efficiency postoperative 90%, follow-up 1.5 to 2 years 67-69%.
Percutaneous retrogasserian radiofrequency therapy
Theoretical basis: The nociceptive fibers in the trigeminal nerve are unmyelinated Aδ and C fibers, which can degenerate at 70-75℃, while the Aα and Aβ fibers, which conduct the sense of touch, are not affected.
Indications: Same as closed surgery.
METHODS: Under X-ray or CT guidance, a radiofrequency needle was inserted percutaneously into the trigeminal ganglion and heated to 65-70 ℃ for 1 minute.
Effect: Immediate relief rate of 96-100% for the recent effect and satisfactory long-term efficacy.
Kanpolat: 1600 patients were followed up from 1 to 25 years, 97.67% had complete relief in the early stage, 57.7% had complete relief after 1 treatment at 5 years of follow-up, and 52.3% had disappearance of pain at 10 years. The pain relief rate after multiple treatments was 94.2%, and 41% of patients with one treatment disappeared after 20 years of follow-up, with a relapse rate of 7.7% after six months and a late relapse rate of 17.4%.
Scrivani: 2150 cases with 6-month follow-up, 92% excellent rate, 83% long-term excellent rate, 27% pain recurrence rate, of which 11% required reoperation and 16% were treated with medication only.
Microvascular decompression of the trigeminal nerve (MVD)
Theoretical basis
Trigeminal neuralgia is caused by pulsatile compression of the sensory roots into the brainstem segment. the REZ area is particularly sensitive to pulsatile and cross-vessel compression, while peripheral nerves outside this segment are less susceptible to microvascular compression pain due to the encapsulation of neuropil cells. In the elderly, due to arterial displacement or lengthening caused by atherosclerosis, vascular compression of the REZ zone, a zone where the Schwann cells of the trigeminal nerve terminate at the brainstem, forms a 0.5- to 1-cm unmyelinated pocket between the central and peripheral myelin sheaths, which is only wrapped by oligodendrocytes. Compression of the microvasculature causes pseudosynapses to form between the nerve fibers of the REZ, resulting in short circuits in conduction.
Indications
Primary trigeminal neuralgia that has failed or recurred with other methods of treatment.
Steps of MVD surgery
The patient is placed in the lateral position, a transverse incision of approximately 5-6 cm in length is made at the level of the external auditory canal, the occipital muscles are separated, and the retractor is propped open. The skull is exposed upward to above the transverse sinus and outward to beyond the sigmoid sinus.
The bones are exposed and drilled, and a bone window is formed, within the size of 3×3 cm; the dura is cut in an arc 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.
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, carefully identify the responsible vessels (offending vessels), mostly arteries, most commonly SCA, followed by AICA, sometimes basilar artery, and even PICA; occasionally venous compression, the veins are most commonly branches of the rock vein.
The arachnoid membrane between the nerve and the vessel is fully released, and an appropriate size of Teflon cotton is placed between them.
If there is no clear offending vessel, a partial cut of the posterior root of the trigeminal nerve is required. The extent of the cut depends on the patient’s symptoms, but the first branch should not be cut.
Surgery method
A.Position
B.Surgical incision and bone window
C.Intraoperative view
Microvascular (arterial or venous compression)
Microvascular to nerve compression
After microvascular decompression
MVD surgical outcome
Recent results
Early surgical results are achieved when the facial pain disappears after the patient is awake from anesthesia, with most reports of 82-95% recent efficiency.
Approximately 40% of patients continue to have varying degrees of pain for several weeks after surgery, which resolves within 2-8 weeks.
Long-term efficacy
Baker: 1185 patients with a mean follow-up of 6.2 years, including a 5-year follow-up rate of 91% and a 6-year follow-up rate of 87%. Unilateral surgery was performed in 1166 cases and bilateral in 19 cases. Postoperatively, 82% had complete relief, 16% had partial relief, and 2% had no effect. After one year, 75% of the pain disappeared completely and 9% of the pain was partially relieved. Ten years after surgery, 70% had complete remission and 4% had occasional pain but did not require medication.
Theodosopoulos: In 420 patients, 87% had complete remission after surgery, with an overall efficiency of 98%. At a mean follow-up of 4.7 years, 93% improved significantly and 72% disappeared completely.
Postoperative recurrence
Between 3 and 20%, postoperative recurrence mostly occurred within the first 1 to 2 years after surgery, with a recurrence rate of less than 2% at 5 years after surgery and less than 1% at 10 years after surgery, and an excellent rate of 85% could still be achieved after reoperation after recurrence.
Factors affecting the long-term efficacy after MVD surgery
Whether the pain is relieved immediately after surgery, if the pain is not completely relieved 2 weeks after surgery, it predicts that the pain is prone to recurrence in the near future.
Those with arterial compression in the trigeminal nerve REZ are less likely to recur, and those with no intraoperative arterial compression or those with venous compression vessels have a high recurrence rate after surgery.
Patients with a history of less than 7 years have a good surgical outcome, and those with a history greater 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 long-term outcome. Those who had previous trigeminal nerve radiofrequency thermocoagulation, trigeminal nerve rhizotomy or with sensory impairment had poor results.
Reasons for recurrence of symptoms after MVD surgery
Intraoperative failure to identify the responsible vessel or inadequate decompression.
Embolization of the ethmoid sinus and obstruction of venous return, resulting in new venous compression.
Arachnoid adhesions at the trigeminal REZ or formation of new adhesions after surgery.
Improper placement or displacement of the interpositor (isolator).
Complications after MVD surgery
These include cerebellar contusion and hematoma, facial palsy, hearing loss, cerebrospinal fluid leakage, facial sensory disturbance, diminished corneal reflex, corneal ulceration, and oral mucosal ulceration.
Stereotactic radiosurgery (gamma knife)
Indications
Same as closure and radiofrequency treatment.
Method
The same as general γ-knife surgery, the selected target location is mainly located at the trigeminal nerve root into the cerebral bridge, and there is also a choice of double target location containing both the trigeminal hemimelia.
Results
McNatt treated 49 patients with a mean follow-up of 49 months, resulting in pain relief in 27 patients (61%).
Sheehan treated 151 patients, of whom 136 received 1 irradiation, 14 received 2 irradiations, and 1 received 3 irradiations, with a mean follow-up of 19 months (2-96 months), resulting in a mean time required for pain relief of 24 days (1-180 days), with 47, 45, and 34% of patients receiving complete pain relief at 1-, 2-, and 3-year postoperative follow-up, 90, 77, and 70% of patients pain partially improved, and 27 of 122 patients who received a single irradiation experienced a recurrence of symptoms.
Care measures
1. Diet should be regular. It is advisable to choose soft and easy-to-chew food. Patients whose pain is induced by chewing should eat a liquid diet, do not eat fried food, should not eat stimulating, too acidic and too sweet food and cold food; diet should be nutritious, usually should eat more vitamin-rich and detoxifying food; eat more fresh fruits, vegetables and legumes, less fatty meat and more lean meat, food should be light.
2, to avoid seizure triggers: eat rinse, talk, brush your teeth, wash your face action should be gentle. In order to avoid inducing the plate machine point and cause trigeminal neuralgia. Do not eat irritating foods such as onions. Pay attention to the warmth of the head and face, avoid local freezing and moisture, do not use too cold or too hot water to wash the face; usually should maintain emotional stability, should not be excited, should not be fatigued and stay up late, often listen to soft music, calm mood, keep enough sleep. Keep a happy spirit, avoid mental stimulation; try to avoid touching the “trigger point”; regular living, indoor environment should be quiet, neat, fresh air. Avoid anxiety caused by the stimulation of the surrounding environment, which may trigger or aggravate the pain.
3. Pain care: Observe the patient’s pain site and nature, understand the causes and triggers of pain, discuss with the patient ways to reduce pain, encourage the patient to use guided imagery, listen to light music, read newspapers and magazines and other distractions to achieve mental relaxation and reduce pain.
4.Medication care: instruct the patient to take painkillers correctly as prescribed by the doctor, and inform the patient of possible adverse reactions, such as carbamazepine may cause dizziness, drowsiness, dry mouth, nausea, unstable walking, liver function impairment, skin rash and leukopenia; some symptoms may disappear on their own after several days, the patient should not change the drug or stop the drug at will, the nurse should observe, record and report to the doctor in time.
5, after trigeminal neuralgia surgery, in addition to general post-operative craniotomy care, attention should also be paid to whether trigeminal neuralgia patients have complications of keratitis and peripheral facial palsy, because the process of surgical free vessels, easy to disconnect or touch the tiny branches that compress the main nerve root of the vessel or the pontine brain, and facial sensory loss.
Health guidance
1.Disease knowledge guidance: The disease can be periodic attacks with a long duration, and the inter-episode period tends to shorten with a longer duration. Patients and family members should be helped to master the knowledge and self-care methods related to the disease to reduce the frequency of attacks and alleviate the patient’s pain.
2, avoid triggers: instruct patients to establish good habits, maintain emotional stability and a happy mood, appropriate distraction, wash face and brush teeth gently.
3.Medication and consultation guidance: follow the doctor’s prescription for reasonable use of medication, check liver function and blood routine every 1-2 months for those taking carbamazepine, and consult the doctor promptly when dizziness, unstable walking or skin rash occurs.
Prognosis
Trigeminal neuralgia rarely heals on its own, and the course of the disease is cyclical, with each attack lasting several days, weeks or months, and the remission period lasting several days to several years, but often shortens with the course of the disease.