Headache Medicine 2021, 12(1) p-ISSN 2178-7468, e-ISSN 2763-6178

ASAA

DOI: 10.48208/HeadacheMed.2021.2

Headache Medicine

Review

Clinical and physiopathological aspects of the glossopharyngeal

neuralgia

Victor Souza Maria Passerini Bianca Sobral Vinicius Baiardi Hilton Mariano da Silva Junior

Department of Neurology, Pontifícia Universidade Católica de Campinas, Campinas, São Paulo, Brazil

Abstract

Introduction

Glossopharyngeal neuralgia is a rare syndrome characterized by paroxysms of unilateral and

severe stabbing pain occurring in the 9th cranial nerve’s distribution. Although other neuralgias

are well described in the medical literature, glossopharyngeal neuralgia and its physiopathology

are scarcely contemplated. The vascular compression at the nerve root entry zone is the primary

explanation for the disease. The rst-line treatment is pharmacological, including carbamazepine,

oxcarbazepine, and gabapentin. Surgical treatment is offered to medication-refractory patients,

and microvascular decompression surgery has presented the best outcomes.

Objective

To investigate the pathophysiological and clinical aspects of the different presentations of glosso-

pharyngeal neuralgia.

Method

A narrative review of literature including case reports and clinical trials were carried out. The

articles were systematically obtained and assessed by the authors.

Results

A search of literature yielded 31 papers that regarded glossopharyngeal neuralgia or its variants.

Among them, eight considered vagoglossopharyngeal neuralgia; and seven focused on the glos-

sopharyngeal neuralgia followed or caused by another disease.

Conclusion

Glossopharyngeal neuralgia is a rare disease and requires further studies on its mechanism

and clinical assessment; the physician needs to know how to distinguish it from its variants and

underlying causes.

Hilton Mariano da Silva Junior

drhiltonm@gmail.com

Edited by

Mario Fernando Prieto Peres

Marcelo Moraes Valença

Keywords:

Glossopharyngeal neuralgia

Drug therapy

Glossopharyngeal nerve diseases

Microvascular decompression

Surgery

Anticonvulsant

Carbamazepine

Received: April 7, 2021

Accepted: July 4, 2021

ASAA

Souza V, Passerini M, Sobral B, Baiardi V, Junior H

Clinical and physiopathological aspects of the glossopharyngeal neuralgia: a systematic review

Introduction

lossopharyngeal neuralgia (GN) is an uncommon crani-

ofacial and pharyngeal pain syndrome characterized by

paroxysms of unilateral and severe stabbing pain occurring in

the 9th cranial nerve's distribution. According to the Interna-

tional Classication of Headache Disease

, glossopharyngeal

neuralgia is a disorder characterized by a severe, transient,

stabbing, unilateral pain experienced in the ear, base of the

tongue, tonsillar fossa and/or beneath the angle of the jaw. It

also involves the pharyngeal and auricular branches of CN X.

The pain may be spontaneous or precipitated by swallowing,

chewing, coughing, or talking. It arises from compression,

demyelination, or dysfunction of the IX or X nerves. Vasomotor,

trophic, or neurovegetative disorders may occur concomitantly

with GN, and central or peripheral nerve compromise may

be present. This neuralgia may be associated with bradycar-

dia, asystole, convulsions, and even life-threatening syncopal

episodes in some patients. GN prevalence is considerably

rare, and its diagnosis presents some challenges given the

diversity of its clinical picture. The rst-line therapy for GN

is pharmacologic, using neuromodulating agents, including

carbamazepine, oxcarbazepine, gabapentin, pregabalin. For

patients with medication-refractory GN, surgical treatment is

an alternative, including microvascular decompression (MVD),

glossopharyngeal and vagal rhizotomy, gamma knife surgery

(GKS), alcohol or glycerol rhizolysis, and pulsed radiofrequen-

cy ablation. Glossopharyngeal neuralgia only represents 0.2-

1.3% of the facial pain syndromes, which requires a careful

investigation during for an accurate diagnosis.

Methods

Articles were obtained through Medline, Embase, and Web of

Science databases. The chosen search terms were “neuralgia”

AND “glossopharyngeal” AND “physiopathology”. These

terms were searched independently by the authors, and they

have found the same number of articles. These researches hap-

pened between 1

and 15

, November, 2020. Only articles

from 2000 to 2020 and written in English or Portuguese were

eligible. Articles reporting GN and associated syndromes

were selected; those that emphasized other diseases were

not included. Book chapters, incomplete articles, technical

reports, and other reviews were not included. The authors

assessed the risk of bias across studies, including trials whose

patients were randomly assigned to the study.

Results e discussion

The primary search identied 158 articles (Figure 1). After

removing 50 duplicates, title and abstract screening of 108

articles yielded 38 articles for full-text reading. A total of 7 full-

text assessed articles were excluded, 5 for addressing other

themes but adult GN, and two had their full-text not found.

The assessment included 31 articles at the nal inclusion.

Figure 1. Description of the systematic articles assessment.

Anatomy of the glossopharyngeal nerve

The glossopharyngeal nerve emerges from the medulla be-

tween the inferior olive and the inferior cerebellar peduncle,

close to the facial and vagus nerves. It exits the skull through

the jugular foramen, along with the vagus and accessory

nerves. Moreover, the internal jugular vein and the internal

carotid artery surround the IX nerve, which courses in front

of the carotid artery. At the jugular foramen, the IX nerve

divides into three branches: the tympanic nerve (Jacobson’s

nerve), its only motor branch, supplying the stylopharyngeus

muscle, and the carotid sinus nerve.

Physiopathology and etiology

According to the ICHD-3

, GN is a disorder characterized

by paroxysms of unilateral severe stabbing pain, with abrupt

onset and termination, in the distributions of the glossopha-

ryngeal nerve and the auricular nerve and pharyngeal

branches of the vagus nerve. It is commonly provoked by

swallow-ing, talking, or coughing.

TThis neuralgia is classied as classical, secondary, or idio-

pathic. The classic GN diagnose relies on the association

of a suggestive clinical picture and the demonstration on

MRI or during surgery of neurovascular compression of the

glossopharyngeal nerve root. The secondary GN is caused

by an un-derlying disease, such as neck trauma, multiple

sclerosis, tonsillar or regional tumors, cerebello-pontine angle

tumors, and Arnold-Chiari malformation.

The

primary GN

mechanism is unclear, although there is a role in vascular

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Souza V, Passerini M, Sobral B, Baiardi V, Junior H

Clinical and physiopathological aspects of the glossopharyngeal neuralgia: a systematic review

compression at the root entry zone (REZ) of the IX nerve.

Even though the posterior inferior cerebral artery (PICA)

rarely crosses the glossopharyngeal nerve, it may make an

upward loop and compress the supraolivary fossette. The

manipulation of a microcatheter and guidewire within the

cerebral arteries showed, for the rst time, that the PICA

compresses IX nerve.

It is known that not only PICA, but the

Anterior Inferior Cerebral Artery (AICA) and the Vertebral

Artery (VA) can be of-fending vessels, which makes the GN

diagnosis considerably challenging before surgery.

Ferroli et

al.

identied, between 1990 and 2007, vascular compres-

sion of the IX nerve in 31 patients with GN. Ac-cordingly, the

compressing vessels are as follows: VA in 7, PICA in 22, AICA

in one, and a vein in one case. Kawashima et al.

also found

their majority offending vessel as arterials, although PICA was

the major vessel in just 10 cases, with the AICA accounting

for 2 cases. Concerning the causes of secondary GN, it is

possible to mention Eagle syndrome (ES), compression by a

tumor, aneurysms, parapharyngeal space lesion, multiple

sclerosis, trauma, malformations, hyperactive dysfunction

syndrome, or post-surgical damages. Many studies

6-13

report-

ed GN with the presence of bradycardia, asystole, syncope,

or seizure. Most cases are due to vagoglossopharyngeal

neuralgia (VGN), which is a rare presentation that accounts

for only 2% of GN cases. The most accepted mechanism for

VGN is that the excessive painful stimuli from the IX nerve

are transmitted through the nucleus of the solitary tract, and

then activates the dorsal motor nucleus of the vagus nerve.

As a result, it will lead to parasympathetic hyperactivity,

inhib-iting sympathetic activity, explaining the bradycardia

and the asystole in VGN.

This vagal reex may also reduce cerebral perfusion, leading

to syncope and seizures in propor-tion to the duration of

asystole.

Nonetheless, seizures are a rare presentation, as

they are a consequence of severe cerebral hypoxia induced

by bradycardia and asystole.

Similarly, the solitary tract nucleus may also activate the facial

nerve and result in a hemifacial spasm (HFS). Thiarawat et

al.

reported a patient with abnormal sternocleidomastoid

muscle spasms, while turning his head to the opposite side of

the neck pain; according to them, the accessory nerve might

have caused the symptom, due to an abnormal synapse with

the glossopharyngeal nerve.

Electron microscopic observations have found that the glosso-

pharyngeal and vagus nerves have a short length and a small

volume of the central myelin portion. This may explain the

low incidence of VGN in the general population. This study

found a positive directly proportional correlation between the

dimension of the central myelin portion and the incidences

of these neuralgias.

Clinical presentation and symptoms

In most common clinical pictures, the onset of GN is subacute,

as patients experience unpleas-ant sensations on one side of

the jaw, inside the mouth, and in the ear. Pain distribution is

usually unilat-eral, shock-like, and with successive attacks of

pain, not only including the glossopharyngeal nerve, since

it may extend to the pharyngeal and auricular branches.

When these vagal branches are involved, vagal-damage

manifestations are more exacerbated, which may include

changes in the voice such as hoarseness and cough. In

uncommon cases, pain may be bilateral, since it is present

on the other side.

15-17

Pain may also be present in the middle ear, ear canal, pos-

terior portion of the oropharynx, retromolar region, throat,

posterior part of the tongue, larynx, and jaw or below the

angle of the jaw. This is generally paroxysmal, from 2 sec-

onds to 2 minutes (average duration is 8 to 50 seconds),

and can wake the patient up during the night. Thus, GN

is divided into two clinical types, based on the distribu-tion

of pain: the tympanic (affects the ear) and the oropharynx

(affects the oropharyngeal area).

In or-der to conrm the

diagnosis, local anesthesia is applied to the pharynx and

tonsils, which may pause paroxysms.

The intervals between attacks and exacerbation of the dis-

ease are from days to years, and they are irregular.

About

10% of patients with excessive GN have vagal effects during

an attack, which can trigger bradycardia, hypotension, syn-

cope, seizures, or even cardiac arrest.

12,18-24

In uncommon

cases, GN may present as syncope without associated

pain

, making diagnosis considerably challenging. In addi-

tion, because of severe GN pain, patients may experience

pallor, followed by hypotension associat-ed with bradycar-

dia. Consequently, this might lead to loss of consciousness

and associated tonic-clonic seizure. Other less common

features are tinnitus, vomiting, dizziness, a feeling of swelling,

involuntary movements, sensory loss of the area innervated

by the glossopharyngeal nerve, sweating, salivation, and

unilateral mydriasis.

Pain attacks may occur spontaneously. Yet, they are usually

associated with a specic trigger-ing stimulus, such as chew-

ing, swallowing, coughing, yawning, sneezing, clearing your

throat, blowing your nose, rubbing your ear, speaking, or

laughing

4,27

. Some patients may experience pain triggered

by sweet, acidic, cold, or hot

, or even turning their heads

to the side.

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Souza V, Passerini M, Sobral B, Baiardi V, Junior H

Clinical and physiopathological aspects of the glossopharyngeal neuralgia: a systematic review

Di󰀨erential diagnosis

Glossopharyngeal neuralgia may be confused with other

conditions, like TN, its main differen-tial diagnosis. Although

TN pain is more intense, the quality of pain in both may be

similar. Besides, trigger zones are more characteristic in TN

than in GN. These diseases prevalently occur unilaterally

and in weeks to months episodes.

GN normally affects the

left side (88%) and TN, the right (58%).

There may also be

similarities in motor and sensory decits associated with them.

Nevertheless, association with multiple sclerosis only occurs

in TN.

Finally, it should be noted that even if both occur

concom-itantly, it is possible to separate them by the distinc-

tion of pain and trigger factors. In TN, infranasal or cheek

pain added to cold or touching face triggers are common.

However, in GN, there is tonsillar fossa and pharynx pain,

added to swallowing triggers.

The superior laryngeal neuralgia diagnosis may be mis-

guiding and challenging, because of the throat pain with an

urge to swallow, talking, swallowing, yawning, or coughing

as triggers like in GN. The nervus intermedius neuralgia, a

further differential diagnosis, is not usually triggered, but

occurs spontaneously, and it is always unilateral.

Eagle syndrome is another differential diagnosis of idiopathic

GN. Both have a diffuse nature of symptoms, and the pain

characterization and location may be similar, but the pain

is more constant in ES, which does not manifest tic-like pain

attacks. Moreover, the physical exam is important to dif-

feren-tiate them

because the distance between the styloid

process tip and the tonsillar fossa is preserved in idiopathic

GN, but it is elongated in the ES.

31,32

Temporomandibular

joint disorders (TMDs) are an im-portant differential diagnosis

when manifested unilateral and intermittently similarly to GN.

There is temporomandibular joint noise in those diseases,

pain on palpation, and worsening pain with chewing.

Swallow syncope may be a differential diagnosis for reex

cardiac syncope by GN, as both oc-cur due to the vasovagal

reex and usually express arterial hypotension. But only in

swallow syncope occur structural and functional esophageal

and cardiac repercussions without pain or insensibility to

swallow.

Finally, ear or sinus infections, dental pain, certain short-last-

ing headaches, and local affections are other possibilities

of GN misdiagnosis.

Pharmacological treatment

Pharmacotherapy is the rst line of treatment for glossopha

ryngeal neuralgia. Using common analgesics is inefcient.

Nevertheless, the most successful medications are anticon-

vulsants. Drug intoler-ance, inefcacy, allergy, or associated

side effects, such as sedation, dizziness, muscle weakness,

cogni-tive impairment, inhibition of bone marrow, and ap-

pearance of dermatological lesions could limit phar-maco-

therapy and may be an indication for surgical treatment.

33,34

Also, a nerve block may be used as a complement to phar-

macological treatment for acute pain, with the administration

of a local anesthetic agent, such as lidocaine (2%) and bupi-

vacaine (0.5%), with or without steroids, ketamine, phenol,

glycerol, and alcohol. Some undesirable effects deserve

attention, such as swallowing difculties and hoarseness.

Finally, it is important to highlight that a bilateral nerv-ous

block may cause vocal cord paralysis.

For vagoglossopharyngeal neuralgia, when syncope epi-

sodes are present, atropine should be used as a drug of

choice. Atropine ceases bradycardia

Notwithstanding,

pain attacks tend to persist. Continued administration of

carbamazepine may decrease painful symptomatology, as

well as heart symptoms

. but it has been known to fail after

initial success.

Using a temporary pacemaker to manage reex cardiac

syncope until ideal therapeutic levels of carbamazepine

were reached was initially proposed in 1971 by Khero and

Mullins.

Regarding the use of a denitive pacemaker, the

literature is controversial. Kazemi et al.

stated that what led

his team to implant a permanent pacemaker in a patient

with syncopal storm caused by glossopharyngeal neuralgia

was based on the efcacy of this therapy in the treatment

of idiopathic carotid hypersensitivity syn-drome and on the

likelihood of future recurrence of GN.

However, it is be-

lieved that the pharmacolog-ical and surgical approaches

make the use of the pacemaker unnecessary.

Surgical Treatment

Surgical treatment is indicated for patients whose pharma-

cotherapy is unsuccessful, for patients with tumors, or those

whose interaction between nerves and vessels causes car-

diac syndrome.

This therapy has been described as better

successful than pharmacological treatment, but with higher

mortali-ty and morbidity rates.

Surgical therapies include MVD, glossopharyngeal and

vagal rhizotomy, GKS, alcohol or glycerol rhi-zolysis, and

pulsed radiofrequency ablation. Furthermore, recurrence

rates are shown to be lowered with the surgical approach.

It is important to highlight that the rhizotomy and the MVD

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Souza V, Passerini M, Sobral B, Baiardi V, Junior H

Clinical and physiopathological aspects of the glossopharyngeal neuralgia: a systematic review

of the IX and the X nerves ensure higher pain relief rates

for GN. MVD has the highest initial and long-term success;

rhizot-omy is a safe and useful backup procedure if MVD is

technically difcult.

Microvascular decompression is very effective in decompress-

ing the REZ.

Immediate pain relief is found in up to 90% of

patients, persisting in 73% of them for 5 years.

Kawashima

et al.

report MVD through transcondylar fossa with positive

results. MVD is also the treatment of choice in the coexistence

of cranial nerve root compression diseases.

Liu et al.

point-

ed to the rst case of the coexistence of HFS and GN. It is

believed that, in this case, MVD is the only option to relieve

the compression of the VII and IX nerves, without permanent

nerve damage, such as in the rhizotomy.

Other surgical techniques are options in the management of

GN. Notwithstanding, they are considered destructive

, such

as glycerol or alcohol rhizolysis, GKS, vagus nerve rhizotomy,

and radiof-requency thermocoagulation. In these procedures,

about 90% of the patients also attended the cessation of

symptoms. However, after 5 years, the pain returns in approx-

imately 50% of them.

Regarding GKS, the surgery is very

expensive, and initial pain relief can take 6 to 8 weeks. The

best results are obtained by special neural images.

For elderly patients, a peripheral glycerol injection is an

option due to the risk of invasive treat-ments in patients that

have some age-related underlying diseases. Yue et al.

had

shown in their study with 21 elderly patients that peripheral

glycerol injection can be applied for GN management in

patients with a trigger zone around the tonsil. The results

indicate that such a method is a safe and effective treatment

for the control of idiopathic glossopharyngeal neuropathy

in elderly patients since, at the last follow-up evaluation, 15

patients were classied as an excellent outcome. Four cases

had a recurrence of pain after 2 and 13 months, and there is

no evidence of glossopharyngeal nerve palsy. Complications

were not observed.

The therapeutic effect of this procedure

is attributed to the toxic effect (demye-lination and axonal

destruction) of glycerol on peripheral nerves. The mechanism

that leads to pain relief is not fully understood but is probably

related to a reduction in afferent entry.

Glossopharyngeal

or vagal rhizotomy is usually reserved for cases where vas-

cular effects are not evident.

Resection of the elongated

styloid process utilizing a minimally invasive approach can

successfully cure pain in swallow syncope.

An important caveat is that methods such as MVD do not

apply to secondary GN. It is in this context that pulsed ra-

diofrequency (PRF) falls. PRF comprises a non-destructive and

minimally invasive neuromodulatory method, which can be

used in the management of neuropathic pain. It can be per-

formed by an extraoral posteromedial styloid approach in

the presence of rigorous hemodynamic moni-toring. Short

radiofrequency energy pulses, supplied at a constant tem-

perature produce central and pe-ripheral neuromodulatory

effects.

The application of PRF to secondary glossopha-

ryngeal neuralgia had been previously described by Shah

et al., in 2003.

Still, like all methods, PRF has its limitations. Bradycardia and

hypotension may prevent com-plete nerve ablation due to

vagal stimulation. Besides, all destructive or ablative neural

procedures pre-sent the risk of neuritis and neurovascular

injury. Radiofrequency thermocoagulation of the glosso-

pha-ryngeal nerve carries the risk of potential damage to

the vagus nerve.

Kandan et al.

recommend in their study

that both PRF and GKS have shown benets in the treatment

of both primary and secondary GN.

Conclusion

This study aims to gather a sizable amount of information

about glossopharyngeal neuralgia, addressing its etiology

and physiopathology to its forms of clinical presentation and

treatment. Further studies over its specic physiopathology,

as well as other glossopharyngeal-related syndromes, are

re-quired. The possibilities of treatment vary from the use of

drugs to surgical intervention in cases of fail-ure in pharma-

cological treatment.

Contribution authors: all authors had the same contribution

Funding: No

Conflict of interests: The authors report no conict of interest

Victor Souza

https://orcid.org/0000-0003-0974-5474

Maria Passerini

https://orcid.org/0000-0002-6096-7171

Bianca Sobral

https://orcid.org/0000-0001-8690-2061

Vinicius Baiardi

https://orcid.org/0000-0002-6976-9577

Hilton Junior

https://orcid.org/0000-0002-9778-9946

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