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Abstract

Background

Isolated neuralgic pain in the deep ear may arise from either nervus intermedius (NIN) or glossopharyngeal (GPN) neuralgias. Current International Headache Society (IHS) International Classification of Headache Disorders, second edition (ICHD-2) criteria for these cranial neuralgias require the presence of a characteristic trigger.

Aim

The aim of this article is to report cases of triggerless neuralgic otalgia to better understand a subset of patients for whom there may be diagnostic uncertainty.

Methods

Methods included an observational cohort series and systematic literature review.

Results

We identified five female patients with a median age at symptom onset of 58 (range: 47 to 73). Our patients generally experienced an excellent clinical response to carbamazepine. Patients were contacted by telephone at a median follow-up duration of seven years (range: four to 32) from symptom onset, at which time carbamazepine-free remissions were reported by five of five (100%) of the patients. A systematic review of the literature on neuralgic otalgia led us to conclude that NIN was most common among young women (age < 50), and GPN across a wider range of ages of either gender. Among surgically validated cases reported in the literature, triggers were frequently absent in NIN, and variably noted in GPN.

Conclusions

We conclude that the presence of a trigger is not fundamental, and may be impractical, to the diagnosis of neuralgic otalgia, but remains important for specificity between NIN and GPN.

Keywords

Cranial neuralgia glossopharyngeal nervus intermedius otalgia triggers

Introduction

The sensory innervation of the ear is complex, including general somatic afferent contributions from cranial nerves V3, VII, IX, and X, in addition to the upper cervical nerve roots (C2 and C3). The auriculotemporal nerve (V3) supplies portions of the tympanic membrane, anterosuperior wall of the auditory canal, and the majority of the helix, including the tragus. VII also innervates the tympanic membrane, in addition to the remaining posteroinferior portions of the auditory canal. The vagus and glossopharyngeal nerves supply the inner aspect of the tympanic membrane. Finally, the upper cervical roots (C2 and C3) supply superficial portions of the external ear, including the lobule (1,2).

The differential diagnosis of neuralgic otalgia is complex and has been associated with an often confusing history of diagnostic ambiguity in the medical literature (3). The International Headache Society (IHS) International Classification of Headache Disorders, second edition (ICHD-2), specifies diagnostic criteria for nervus intermedius (NIN) and glossopharyngeal (GPN) neuralgias, which may both be associated with deep neuralgic ear pain (3 –5). However, diagnosis of either NIN or GPN necessitates the presence of a characteristic trigger.

We report five cases of triggerless neuralgic otalgia to better understand this subset of patients who have not been previously studied and for whom there may be diagnostic uncertainty. Further, we performed a systematic review of the literature to identify clinical features of predominant otalgia as a manifestation of surgically validated NIN and GPN.

Methods

Five cases were identified from the case records of the Mayo Clinic headache registry of isolated neuralgic otalgia, fulfilling all but the ICHD-2 criterion of a characteristic trigger for NIN (i.e. auditory canal stimulation), or GPN (i.e. swallowing). All cases were evaluated at our institution by a headache specialist (FMC). Study inclusion further required that dedicated magnetic resonance imaging (MRI) be pursued to exclude an alternative etiology. Patients were contacted by one of the study investigators (JHS) by telephone to extend the clinical follow-up.

We then reviewed the English-language literature by searching PubMed through October 31, 2012 (0900), using the search terms “nervus intermedius neuralgia,” “geniculate neuralgia,” “Hunt’s neuralgia,” “facial nerve neuralgia,” “tic douloureux of the chorda tympani,” “glossopharyngeal neuralgia,” and “vagoglossopharyngeal neuralgia.” The bibliographies of papers identified through MEDLINE searches were also reviewed to identify additional relevant articles. We sought to identify all surgically validated cases of isolated (or overwhelmingly predominant) otalgia secondary to either NIN or GPN. Cases of NIN and GPN, in which surgical validation of diagnosis was confounded by multiple nerve/root sections were excluded, including those previously reviewed by Bruyn (3,5). However, in contrast to Bruyn, we did allow for cases of NIN with concurrent sectioning of the VIIIth nerve, given that this nerve either carries no nociceptive fibers, or may carry the pain fibers of the nervus intermedius (6). Cases of symptomatic neuralgias were excluded. The main outcomes of our literature review were to identify the demographic associations (age at symptom onset, gender) and frequency of triggers of otalgia as reported among patients with NIN and GPN. For articles in which only sparse clinical data were reported, the authors of the publications were contacted in an effort to obtain more complete information. If the authors could not be reached, or could not supply adequate supplemental information, articles were excluded.

Results

Case series

Four out of our five patients were initially evaluated at our institution subsequent to the publication of the IHS ICHD-2 criteria. The clinical features are summarized in Table 1. The median age at symptom onset was 58 (range: 47 to 73), with five of five (100%) patients being female. All patients denied triggers that were asked about systematically, including swallowing, touch (including use of an auditory canal cotton swab), wind, yawning, chewing, and talking. All specifically denied pain in the throat or tonsillar fossa.

Table 1.

Clinical features of patients with triggerless neuralgic otalgia (n = 5).

Case	Age at initial symptom onset/ gender	Location	Radiation	Quality	Intensity	Triggers	Relieving factors	Attack frequency	Associated symptoms	Clinical course
1	52/F	Deep, left ear	Pre-auricular	Jabbing	Severe	None	None	Daily; “dozens” of brief jabs throughout the day	None	Relapses at ages 67, 70, and 74, with interval CBZ-free remission. No relapses at last follow-up (age 84).
2	58/F	Deep, right ear	None	Jabbing/sharp/ burning	Severe	None	None	Three to four days per month; one to two hours of jabs per day	Subjective decreased hearing (ipsilateral) (normal audiogram)	CBZ-free remission at last follow-up (age 63).
3	47/F	Deep, right ear	Occasional paresthesias in the right cheek	Jabbing/sharp	Severe	None	None	Daily; ∼ 200 jabs/day	None	CBZ-free remission at last follow-up (age 52).
4	73/F	Deep, left ear	Occasional sharp pains in throat	Jabbing/sharp	Severe	None	None	Daily; “dozens” of jabs per day	None	CBZ-free remission beginning at age 77 through last follow-up (age 80).
5	70/F	Deep, right ear	None	Jabbing/sharp	Severe	None	None	Daily × one week (“frequent”), spontaneous remission	None	Relapse at age 74, lasting one week. CBZ-free remission at last follow-up (age 75).

F: female; CBZ: carbamazepine.

The clinical course was generally characterized by relapses and remissions. Remissions were observed either spontaneously (case 5), or following withdrawal of carbamazepine (CBZ) (cases 1, 2, 3 and 4). Relapses were often separated by several years.

Relevant co-morbidity in our cohort included polymyalgia rheumatica (PMR) (case 1), prior history of breast cancer status-post bilateral mastectomies (case 2), bilateral temporomandibular osteoarthritis (case 3), and frequent episodic migraine without aura, well controlled with amitriptyline 50 mg nightly (case 4). In case 4, there was thought to be an increased breakthrough of episodic migraines, triggered by the relapses of neuralgiform ear pain.

Comprehensive neurologic examination was normal in all five patients. MRI with and without gadolinium studies were reviewed in all patients, with the scans of four patients (cases 2–5) including Fast Imaging Employing Steady State Acquisition (FIESTA) T2-weighted images examining the posterior fossa. MRI of cases 1, 3, and 5 were normal. Case 2 had a partial empty sella. Case 4 had tortuosity of the basilar artery, indenting the left pontomedullary junction ventrally, ipsilateral to the otalgia. However, no neurovascular contact point was observed. Cases 1–4 had normal serum measurements of both erythrocyte sedimentation rates and C-reactive protein. A positive Varicella Zoster immunoglobulin G (IgG) (but not IgM) was noted in case 1. Two patients underwent screening audiograms that were normal (cases 2 and 4). Because of the history of PMR, case 1 underwent a temporal artery biopsy as part of her evaluation, which was negative.

Abortive treatments with either over-the-counter nonsteroidal anti-inflammatory drugs or acetaminophen were found to be ineffective by four of four patients in whom these were utilized. Opioids were trialed as abortive agents by two patients, in whom they were found to be ineffective. CBZ was the only prophylactic medication utilized in our cohort, at a median effective dose of 900 mg (range: 400 to 1200 mg). CBZ use was associated with complete remission of pain in three patients, and significantly improved pain in one patient (case 4) in whom dose escalations were limited by side effects (sedation) and hyponatremia. In case 5, relapses were too brief to warrant a preventive treatment. No patient underwent an interventional procedure for the otalgia.

At a median telephone follow-up duration of seven years (range: four to 32) from symptom onset, sustained CBZ-free remissions were reported by five (100%) of the patients.

Systematic literature review

We identified 15 cases of surgically proven NIN (Table 2) (7 –20). In instances where there were missing data, authors often no longer had access to the original records, were not able to be reached, or had since passed away, as was the case with Dr. Jack Pulec’s single-authored series of 64 patients with geniculate neuralgia (18). Unfortunately, without even a mention of the ages and genders of the patients, only a single patient could be included from this latter series. In our cohort identified from the literature, 14/15 (93.3%) were female, with a median age at symptom onset of 41 (range: 16 to 47). A trigger was present in three, absent in seven, and not mentioned in five. In the three with triggers, noise was a trigger in one, and palpation of the auditory canal in two. In seven of 15 (46.6%) of cases, radiation was reported in distributions considered more typical of trigeminal neuralgia, and even occipital in some cases. Median follow-up was 18 months (range: three to 280).

Table 2.

Predominant otalgia as a feature of surgically validated cases of nervus intermedius neuralgia.

No. patients Reference	Age at symptom onset/gender	Reported clinical features	Triggers	Associated symptoms	Treatment/follow-up/outcome
N = 1 Clark and Taylor, 1909 (7)	26/F	“Neuralgic pain” in front of left ear, “steady pain” in the depths of the ear, in the anterior wall of the auditory canal. More mild neuralgic pains noted in all trigeminal and occipital regions.	None	None	Cured by section of NI/VII/VIII, follow-up: five months.
N = 1 Furlow LT, 1942 (8)	X^a/F	Lightning pains in left ear, deep (Occasional radiation to left eye).	Touch of a “very small area” in the upper-posterior wall of the external auditory canal close to tympanic membrane.	None	Cured by NI section, follow-up: one month.
N = 1 Wilson AA, 1950 (9)	46/F	Prior history of “sick headaches.” Acute onset of deep, continuous aching pain in ear radiating to the cheek, eye.	None	None	Section of V2, retrogasserian neurectomy brought initial complete relief. Pain returned. Remission following section of NI, follow-up: 18 months.
N = 2 Rosen S, 1953 (10)	1: X^a/F; 2: 26/F	1: Lancinating pain, deep, left ear and “entire pinna.” Episodes (one to 12 hours), occurring four times per week to three times per month. 2: Daily attacks of pain in deep, right ear.	1, 2: None, except for surgical nerve stimulation.	1: “Pressure and heaviness in the head” 2: Tinnitus, “slight vertigo,” bitter taste	1, 2: Cured by section of the chorda tympani.
N = 1 (total series = 4) Sachs E, 1968 (11)	44/F	History of chronic right-sided headaches (features not described) with narcotic dependence, “emotionally unstable.” One-year history of lancinating pain in right ear.	None	None	Intraoperative stimulation of VIII reproduced pain. Cured with section of VIII, follow-up 15 years.
N = 1 (out of 10 in series) Yeh H, 1981 (12)	38/F	Right-sided neuralgia otalgia	Not reported	Hemifacial spasm, decreased hearing.	Cure of neuralgia and hemifacial spasm with MVD, follow-up: two years, eight months.
N = 1 Yeh H and Tew Jr JM, 1984 (13)	34/F	Constant, aching pain in right ear, radiation into cheek and occipital region. Decreased hearing.	None	Hemifacial spasm (4 years after onset of otalgia)	Cure of neuralgia with MVD, follow-up: four years.
N = 1 (out of 18 in series) Rupa V et al., 1991 (14)	27/M	Sharp, paroxysmal left ear pain	Noise	Tinnitus, vertigo	Cured by section of NI and GG, follow-up: five years.
N = 1 Young RF, 1992 (15)	41/F	Severe pain in deep, right ear, radiation along mandible. Increased sensitivity of mandibular teeth.	None	None	Cured with MVD, follow-up: three months.
N = 1 Alcaraz N et al., 1999 (16)	47/F	“Unilateral otalgia for 12 months”	Not reported	Not reported	Cured by endoscopic-assisted section of the nervus intermedius, follow-up: 4 months.
N = 1 King WA et al., 2001 (17)	46/F	Right-sided otalgia × 12 months	Not reported	Not reported	Pain remission after MVD, follow-up: three months.
N = 1 (total series = 64) Pulec J, 2002 (18)	45/F	“Ice-pick” in left ear, two to three episodes per day, lasting 3 minutes.	Not reported	Sensation of left eye spasm.	Cured with excision of NI and GG, follow-up: two years.
N = 1 Sakas DE et al., 2007 (19)	46/F	“Paroxysmal pain involving the auditory canal, pinna, and retromastoid area.”	Not reported	Tinnitus, hearing loss, unsteadiness.	Cured with MVD, follow-up: six months.
N = 1 Saers SJF, 2011 (20)	16/F	Stabbing pain, deep left ear, lasting “minutes to hours.”	Palpation of posterior wall of auditory canal.	None	Cured with MVD, follow-up: one year.

Age not stated in manuscript. F: female; NI: nervus intermedius; MVD: microvascular decompression; GG: gasserian ganglion.

We identified 14 cases of surgically proven GPN with predominant or exclusive otalgia (Table 3) (21 –30). Nine of these patients were female, with a median age of symptom onset of 37.5 (range: 15 to 62). Triggering of ear pain was reported in 11/14 (78.5%) of the cases, most often by swallowing. In one case, the characteristic trigger did not emerge until 36 years after symptom onset (21). Touching the ear was actually noted as a trigger for GPN in three separate reports (22,24,29). Radiation into the trigeminal nerve distribution was noted in six of these cases. Median follow-up was six months (range: 10 days to 94 months).

Table 3.

Predominant otalgia as a feature of surgically validated glossopharyngeal neuralgia.

No. patients Reference	Age at symptom onset/gender	Reported clinical features	Triggers	Associated symptoms	Treatment/follow-up/outcome
N = 1 Jefferson G, 1931 (21)	34/M	“Paroxysmal pain” deep in left ear, radiation to pre-auricular region × 36 years. Initially, two attacks per year, and then every four months (age 70).	None × 36 years, then swallowing, in association with developing throat pain (age 70).	None	Cured with avulsion of IX. Follow-up: 15 months.
N = 1 Keith WS, 1932 (22)	46/F	“Boring” pain deep in right ear, involving lobule, some radiation to throat.	Swallowing, “digital pressure…within 2 inches of the…auditory canal produced spasm”	None	Cured with avulsion of IX. Follow-up: 10 days.
N = 1 Reichert FL, 1934 (23)	31/F	Deep, stabbing left auditory canal. Constant, aching left-sided headache.	None	“Sensitiveness of the mastoid and pre-tragal regions”	Cured (both ear pain and headache) with section of IX, follow-up: four months.
N = 1 Lillie HI, 1936 (24)	15/F	Stabbing pain in deep left ear and dull, continuous left-sided headache.	Stimulation of the posterior wall of the external auditory canal.	Diminished hearing in left ear.	Cured with section of IX, follow-up: six weeks.
N = 1 Cuneo HM, 1943 (25)	33/M	“Flash of pain” in front of right ear, with paroxysmal burning inside, lasting seconds.	Swallowing	None	Cured with rhizotomy of IX, follow-up: “to date there has been no recurrence,” publication was within three months of surgery.
N = 1 Svien JH et al., 1957 (26)	37/M	Stabbing, burning in left ear. Occasional paresthesias in front of left ear, and along mandible.	Swallowing, occasionally by talking or brushing teeth.	Syncope	Cured with section of IX/upper rootlets of X, follow-up: six months.
N = 4 (total series = 18) Bohm E and Strang RR, 1962 (27)	All female Ages: 53, 55, 57,27	“Deep” in ear (n = 3), “external auditory canal” (n = 1)	Swallowing (n = 4)	Dizzy attacks (n = 2)	All four underwent surgery, two cured, one with occasional ear pain, and one with “pressure sensations around ear”. Median follow-up for four cases: five years (range: five to seven).
N = 1 (total series = 6) Laha RK and Jannetta PJ, 1977 (28)	59/M	Stabbing pain in deep left ear, some radiation to left side of face and pharynx.	None	“Hypesthesia V2, decreased hearing left ear”	Cured with MVD and section of IX/upper rootlets of X, follow-up: 2.5 years.
N = 2 (total series = 9) King J, 1987 (29)	1: 20/F; 2: 38/F	1: Tingling behind right ear, stabbing pain in right tragus, radiation along jaw. 2: Stabbing/constant ache deep in left ear, radiation to left forehead, cheek.	1: Swallowing 2: Swallowing, touching left ear	None	1: Division of IX, carbamazepine, residual mild ear pain, follow-up: three years. 2: Cured with division of IX/X, follow-up: two months.
N = 1 (total series = 14) Martínez-Gonzáles JM et al., 2011 (30)	62/M	1: “Strangulation,” ∼ 30-second bursts of pain in ear.	Not reported	Not reported	Not reported

M: male; F: female; MVD microvascular decompression.

Discussion

These cases highlight the often blurred margins that can exist between cranial neuralgias manifesting predominantly with otalgia (7,23). Given that our cases of triggerless neuralgic otalgia met all but one ICHD-2 criteria for both NIN and GPN, we consider our patients to have had “probable nervus intermedius or glossopharyngeal neuralgia.” The patient described as case 4 likely had GPN, given the occasional report of throat radiation. Further diagnostic clarification could have been pursued through cocainization of the tonsillar fossa (31); however, this did not preclude appropriate and successful nonsurgical management in all cases. The distinction between these entities is not trivial, as surgical intervention in NIN may be complicated by hearing loss, and in GPN by reflex bradycardia/asystole (31,32). Further, a dedicated MRI study is mandatory in all cases to rule out structural secondary cases.

Our current understanding of otalgia secondary to either NIN or GPN is limited. This is disappointing given the existence of multiple surgical series that do not elaborate on clinical findings. We utilized strict inclusion criteria in our literature review, although a limitation was inclusion of only the English-language literature. We observed NIN to be most common among young women (age < 50), and GPN to occur over a wider range of ages of either gender. Ear pain alone in GPN has been observed between 2.7 (surgically confirmed) and 9.2% of patients in a large cohort series of 217 cases (31). In cases of suspected GPN, Bohm and Strang have observed that individuals with onset of pain in the ear tend to be younger (50 versus 57 years) (27). Notably, among surgically validated cases of predominant otalgia reported in the literature, triggers were generally absent or not reported in NIN, and only variably noted in GPN. Along these lines, Reichert noted in describing “Jacobson’s plexus tic douloureux of the glossopharyngeus” that the ear pain was “not induced by any movement of the pharynx or tongue” (23). Therefore, most of the surgically validated cases of NIN, and many of other surgically validated cases of GPN reported in the literature, would not satisfy current ICHD-2 criteria. The possibility that the triggers when present in NIN may lie deep within the posterior inferior auditory canal or on the tympanic membrane itself make probing for the trigger to satisfy diagnostic criterion often impractical and may carry risk of injury to the tympanic membrane.

The frequent spread of neuralgia into trigeminal and extra-cranial sensory zones was not uncommonly reported in both cases identified from the literature, and in our own series. The observation of radiation into other dermatomal distributions led Harvey Cushing to refer to geniculate neuralgia as a “pseudotrigeminal neuralgia” (33). The mechanisms underlying this observation are not known, but may reflect central relays within the brainstem. Along these lines, sectioning of the NIN has been utilized as a surgical treatment for medication-refractory chronic cluster headache (34). Another possibility to be considered is that GPN and trigeminal neuralgia are well known to be able co-exist (35). In our patients, we feel that a diagnosis of trigeminal neuralgia is extremely unlikely, given the lack of any facial pain whatsoever, and no typical progression over the follow-up period. Isolated trigeminal deep otalgia has not been reported, even among patients with auriculotemporal neuralgia (32,36). Accurate diagnosis with confirmatory nerve blocks is therefore mandatory for patients being considered for surgical interventions.

Cranial neuralgias are presumed to share a common pathophysiology with ephaptic transmission between fibers mediating light touch and pain accounting for the characteristic triggering of neuralgic pain (37). The frequent observation of demyelination in the trigeminal nerve root entry zone in multiple sclerosis-associated trigeminal neuralgia supports this concept, as these fiber types are in close anatomic proximity in this region (37). Neurovascular compression, notably absent from our cases, is thought to further promote the generation of aberrant impulses. We speculate that differences in the anatomic relationships between cutaneous and nociceptive fibers may protect against ephaptic transmission (i.e. triggering) in our cases of NIN and GPN. Further study of individuals with cranial neuralgias with or without triggers provides an opportunity to further understand disease pathophysiology.

Conclusions

We report individuals with triggerless neuralgic otalgia not classifiable by current ICHD-2 criteria. Our patients experienced excellent clinical outcomes with CBZ treatment. In a systematic literature review of NIN and GPN, we note that a trigger is often not present. We propose that a characteristic trigger is not fundamental to the diagnosis of either NIN or GPN, and should be changed from a required to adjunctive criterion. Because surgery may be required, cocainization of the tonsillar fossa may be required in cases when the diagnosis of GPN is uncertain.

Clinical implications

Neurologic causes of deep ear pain include nervus intermedius and glossopharyngeal neuralgias.

Current criteria require the presence of a characteristic trigger for diagnosis.

We report individuals with neuralgic ear pain without a trigger.

We performed a systematic literature review, showing that even among surgically validated cases, triggers are not common.

Footnotes

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Conflict of interest

None declared.

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Triggerless neuralgic otalgia: A case series and systematic literature review

Abstract

Background

Aim

Methods

Results

Conclusions

Keywords

Introduction

Methods

Results

Case series

Systematic literature review

Discussion

Conclusions

Clinical implications

Footnotes

Funding

Conflict of interest

References