The superior laryngeal nerve is a branch of the vagus nerve that emanates from the inferior border of the conjunctival ganglion, and divides into two branches when it reaches the plane of the greater horn of the hyoid bone. The inner branch crosses the lingual nail membrane and is distributed in the mucosa of the supraglottis area, which is responsible for the sensation of the mucosa there, and injury can cause choking and aspiration; the outer branch mainly innervates the movement of the cricothyroid muscle, so injury can cause a decrease in pitch.
There are reports of secondary factors such as tumor, trauma, surgery, etc. that damage the supraglottic nerve and cause secondary supraglottic neuralgia, while simple primary supraglottic neuralgia has been rarely reported. When the etiological diagnosis is unclear, conservative treatment with carbamazepine drugs and symptomatic treatment with local anesthetic block are often given, with poor long-term results.
1. Diagnosis and differential diagnosis of supraglottic neuralgia.
It is the rarity of the onset of supraglottic neuralgia that leads to the existence of misdiagnosis. A correct diagnosis of supraglottic neuralgia can help in proper management as well as avoiding unnecessary medical manipulation. Supraglottic neuralgia is a sharp, burning, slashing pain originating from the thyroglossal membrane on one side of the larynx and radiating into the ipsilateral mandible and external auditory canal.
Pain episodes are intermittent, lasting from a few seconds to a few minutes per episode, and in severe cases can last for several hours. The pain is intense, with frequent episodes that are triggered by swallowing, speaking, or turning the head, and occasionally bilateral. Since there is no other nerve distribution around the thyroglossal membrane, pain that begins in this area can often help determine supraglottic neuralgia. The trigger point is usually located in the area of the thyroglossal periosteum (where the internal branch of the superior laryngeal nerve crosses the thyroglossal periosteum) and in the pyriform fossa (a fossa formed by the subduction of the mucosa between the superior edge of the epiglottis and the plane of the lower edge of the cricoid cartilage).
Typical trigger point tenderness can aid in early diagnosis, while dicaine spray of the pear-shaped crypt and local block of the superior laryngeal nerve to relieve pain can help establish the diagnosis.
Supraglottic neuralgia is mainly distinguished from glossopharyngeal neuralgia, which is characterized by a brief but intense sharp pain, pins and needles, or burning sensation in one side of the throat, pharyngeal wall, tonsillar fossa, soft palate, and posterior 1/3 of the tongue, with trigger points located in the tonsillar crypt, palate, etc., and radiating into the mouth or ear. The source of pain and trigger point sites are higher than those of supraglottic neuralgia.
2. Exploration of etiology and pathogenesis.
According to the different causative factors, supraglottic neuralgia can be divided into two types: primary (central) and secondary (peripheral). The most common pathogenic factors of secondary (peripheral) supraglottic neuralgia include supraglottic neuritis, which is often caused by upper respiratory tract infections (influenza, laryngitis, etc.) involving the larynx; thyroiditis; laryngeal surgery; tonsillectomy; microscopic neurosurgery; tissue scars after carotid endarterectomy; trauma; congenital disorders including hyoid deviation extrusion; lateral laryngeal diverticulum, etc. These etiologies cause pain due to intrusion of the supraglottic nerve.
The primary supraglottic neuralgia is caused by severe and persistent pain of the thyroglossal membrane after a review of the medical history and various examinations such as MRI of the craniocervical junction area, thyroid ultrasound and laryngoscopy, excluding secondary factors such as tumors, inflammation, history of surgical trauma in the craniocervical junction area and congenital mutations of the larynx. Primary (central) supraglottic neuralgia is rarely reported in the literature, and the etiology and mechanism are not well studied.
It may be related to compression of the superior vagus nerve fibers during their journey away from the brainstem and through the subarachnoid space out of the jugular foramen. We hypothesize that the pathogenesis of primary supraglottic neuralgia may be the same as that of trigeminal neuralgia, facial spasm, and glossopharyngeal neuralgia, in which the same vascular compression of the vagus nerve exiting the brainstem area causes demyelination changes and pseudosynaptic transmission at the site of the axon without the Shewan’s cell sheath, leading to pain production. This was confirmed by the significant compression of the vagus nerve root filaments out of the brainstem area by blood vessels and the complete disappearance of pain after decompression surgery found in this group of cases.
3. Treatment.
Similar to trigeminal neuralgia and glossopharyngeal neuralgia, early oral carbamazepine is one of the effective methods for the treatment of supraglottic neuralgia. For patients for whom drug treatment is ineffective, external block of the supraglottic nerve is also effective in the short term. In case of persistent pain that cannot be relieved for a long time by the above treatment, peripheral supraglottic neurectomy is feasible for secondary supraglottic neuralgia, but certain dysfunction may occur; for primary supraglottic neuralgia, posterior sigmoid sinus approach with microvascular decompression or upper vagus nerve root filament cut can be tried, which can achieve good results.
4.Clinical procedure selection.
In the microvascular exploration of primary supraglottic neuralgia, in view of the mutual anatomical relationship between the vagus nerve and the brainstem, the rock bone and the responsible vessels, we believe that decompression can be performed in all patients who can be decompressed simply by using the operator’s microscopic decompression skills combined with the vascular conditions and where adequate decompression is expected.
In many cases, the close relationship between the posterior inferior cerebellar artery and the vertebral artery and the linguopharyngeal, vagus, and paramedian nerves at the level of the pontine medulla and the high variability of encircling and penetrating conditions make decompression difficult. In addition, the narrow lumen of the craniocervical junction area, the large density of blood vessels and nerves, and the mutual extrusion of blood vessels, nerves and root filaments are not conducive to adequate decompression of blood vessels and nerve roots.
Therefore, in the following cases.
1, the posterior inferior cerebellar artery is combined with the vertebral artery compression, the vascular density is large, the effective decompression space is small, and many vessels cannot push away from the nerve root to achieve adequate decompression;
2.The posterior inferior cerebellar artery is tortuous around the nerve root and the vertebral artery is very elastic, so the compression cannot be released;
3, the lateral segment of the posterior inferior cerebellar artery is hidden in the ventral part of the nerve and the posterior lateral sulcus of the medulla oblongata, which is difficult to pull and separate;
4.The posterior inferior cerebellar artery medullary cerebellar peduncle segment runs between the linguopharynx and vagus, which cannot be fully decompressed;
5, no vascular compression or venous type vascular compression. The linguopharyngeal nerve and the upper root filaments of the vagus nerve can be severed from one side.
Why cut the upper root filament of the vagus nerve? The superior laryngeal nerve is a branch of the vagus nerve emanating from the inferior border of the conjunctival ganglion and is divided into two branches: the inner and outer branches. The inner branch crosses the lingual nail membrane and is responsible for the sensation of the mucosa in the supraglottis region, which is derived from the sensory fibers of the vagus nerve and is directly related to the supraglottic neuralgia; the outer branch mainly innervates the movement of the cricothyroid muscle. Electrophysiological monitoring of the upper and lower root filaments of the vagus nerve revealed that the lower root filaments of the vagus nerve were related to movement and the upper root filaments were related to sensation. Therefore, cutting the upper root filaments of the vagus nerve, which is the sensory branch, can effectively relieve pain.
How many bundles of the upper vagus filaments can be cut to relieve pain and minimize functional impairment? The most ideal way to determine the motor and sensory branches of the vagal root filaments is through electrodes inserted by percutaneous laryngeal puncture or electrophysiological monitoring using electrodes on the surface of the tracheal tube. In the absence of electrophysiological monitoring, we recommend that, because supraglottic neuralgia is a vascular compression of the vagus nerve, it is recommended that the number of bundle branches of the vagus nerve be increased by one bundle branch (1+X) for supraglottic neuralgia surgery compared to the number of upper vagus root filaments cut (X) for glossopharyngeal neuralgia surgery.
In other words, in the combined linguopharyngeal neuralgia surgery, when there are more vagus nerve filaments, at least 1~2 upper vagus nerve filaments should be cut; when there are fewer and thicker vagus nerve filaments, only the upper one filament should be cut or partially cut; while in the supraglottic neuralgia surgery, when there are more vagus nerve filaments, at least 3 upper vagus nerve filaments should be cut; When the vagus nerve filaments are less and thicker, at least 1 and a half filaments should be cut in the upper part to achieve good results.
In the two cases where the vagus nerve could not be fully decompressed, the upper part of the vagus nerve was cut by more than 3 filaments on one side.
Is the linguopharyngeal nerve cut? The hyohypopharyngeal nerve and the vagus nerve are interrelated in the pathogenesis of pain. In particular, the pharyngeal plexus, which is distributed in the pharyngeal muscles and pharyngeal mucosa, is composed of both the pharyngeal branch of the linguopharyngeal nerve and the pharyngeal branch of the vagus nerve, so the two nerves are intertwined in the mechanism of pain onset.
It is also believed that the pain in the deep surface of the external auditory canal and below the angle of the jaw in the painful linguopharyngeal neuralgia originates from the Eustachian branch of the vagus nerve, so it is called “vagal linguopharyngeal neuralgia”. It can be seen that the linguopharyngeal nerve and the vagus nerve are inseparable and communicate with each other in the mechanism of pain pathogenesis. Therefore, we also recommend combined linguopharyngeal nerve dissection in the upper root filament of the vagus nerve for supraglottic neuralgia.
In conclusion, the incidence of primary supraglottic neuralgia is extremely low, and the correct diagnosis of primary supraglottic neuralgia is crucial when secondary factors are excluded. In cases where conservative drug therapy and local anesthetic blockade are ineffective, selective vagus nerve decompression with microvascular decompression and linguopharyngeal nerve dissection in combination with multiple bundles of upper vagus nerve filaments are safe and effective methods for the treatment of primary supraglottic neuralgia.