Glossopharyngeal Neuralgia

Spurling, R. Glen; Grantham, Everett G.

doi:10.1097/00007611-194205000-00014

Cited by 13 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In cases where the diagnosis is in doubt the presence of a trigger spot in the pharynx, stimulation of which produces the typical symptoms, is highly suggestive of the condition (Roulhac and Levy, 1950;Rush ton, i960). The diagnosis is strengthened if this response is abolished by anaesthetizing this trigger spot with a local anaesthetic agent (Adson, 1924;Reichert, 1933;Spurling and Grantham, 1942;Pastore and Meredith, 1949;Thomson, 1954;Rushton, i960).…”

Section: Discussionmentioning

confidence: 99%

“…Surgical treatment for glossopharyngeal neuralgia has been undertaken for fifty years and four different operations have evolved. The cardiac irregularities are thought to be due to abnormal impulses in the glossopharyngeal nerve producing their effect by either of two pathways: (1) by direct excitation of the dorsomotor nucleus of the vagus in the midbrain, subsequent efferent impulses passing along the vagus nerve; (2) by means of a local reflex arc involving the peripheral part of the nerve and its branches to the carotid body and sinus (Ray and Stewart, 1948;Stowell and Gardner, 1952;Richberg and Kern, 1953;Kong et al, 1964;Khero and Mullins, 1971;Garretson and Elvidge, 1962). The convulsions may also be related to abnormal stimulation of the carotid sinus and its subsequent malfunction.…”

Section: Discussionmentioning

confidence: 99%

“…In the remaining five it was ineffective. The attacks were temporarily relieved by local anaesthetic techniques in eight of the cases; by surface application of a local anaesthetic agent to the trigger spot in six (Karnosh, Gardner and Stowell, 1947;Ray and Stewart, 1948;Roulhac and Levy, 1950;Stowell and Gardner, 1952;Lennartz, 1953;Svien, Hill and Daly, 1957), by injecting the nerve in one (Kong et al, 1964) and by injecting the carotid sinus in another (Paillas,Sedan and Allegre,i960).…”

Section: -None Seizuresmentioning

confidence: 99%

See 2 more Smart Citations

Glossopharyngeal neuralgia with syncope

et al. 1977

View full text Add to dashboard Cite

Thirty-two cases of glossopharyngeal neuralgia complicated by syncope, cardiac arrhythmias or convulsions, singly or together, have been reported in the world literature. A further case is described and the clinical features of these thirty-three are reviewed. It is recommended that treatment should be undertaken as a matter of urgency. In the first place, Carbamezapine, with often the addition of Atropine, may prove effective. However, surgical intervention appears to give a better chance of permanent relief. Four alternative methods of surgery are discussed and the cervical or the intracranial approach recommended. Surgery should not be delayed in patients who fail to respond to medical treatment or in whom recurrence of symptoms occurs.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: -None Seizuresmentioning

confidence: 99%

See 1 more Smart Citation

Glossopharyngeal neuralgia with syncope

et al. 1977

View full text Add to dashboard Cite

show abstract

“…The overall incidence of GN appears to be considerably lower than that of TN and is estimated at 0.2-0.7 cases per 100,000 person-years 25 and 0.062/100,000 (Fig 7). 58 However, some authors believe that the true incidence of GN may be higher due to lack of awareness of the disease and difficulties in diagnosis. In general, GN is caused by NVC, while in a minority of cases, trauma, neoplasms, infection, or an elongated styloid process (Eagle syndrome) can be identified.…”

Section: Glossopharyngeal Nerve (Cn Ix)mentioning

confidence: 99%

Imaging of Neurovascular Compression Syndromes: Trigeminal Neuralgia, Hemifacial Spasm, Vestibular Paroxysmia, and Glossopharyngeal Neuralgia

Haller

Etienne

Kovari

et al. 2016

American Journal of Neuroradiology

188

100

View full text Add to dashboard Cite

SUMMARY: Neurovascular compression syndromes are usually caused by arteries that directly contact the cisternal portion of a cranial nerve. Not all cases of neurovascular contact are clinically symptomatic. The transition zone between the central and peripheral myelin is the most vulnerable region for symptomatic neurovascular compression syndromes. Trigeminal neuralgia (cranial nerve V) has an incidence of 4 -20/100,000, a transition zone of 4 mm, with symptomatic neurovascular compression typically proximal. Hemifacial spasm (cranial nerve VII) has an incidence of 1/100,000, a transition zone of 2.5 mm, with symptomatic neurovascular compression typically proximal. Vestibular paroxysmia (cranial nerve VIII) has an unknown incidence, a transition zone of 11 mm, with symptomatic neurovascular compression typically at the internal auditory canal. Glossopharyngeal neuralgia (cranial nerve IX) has an incidence of 0.5/100,000, a transition zone of 1.5 mm, with symptomatic neurovascular compression typically proximal. The transition zone overlaps the root entry zone close to the brain stem in cranial nerves V, VII, and IX, yet it is more distal and does not overlap the root entry zone in cranial nerve VIII. Although symptomatic neurovascular compression syndromes may also occur if the neurovascular contact is outside the transition zone, symptomatic neurovascular compression syndromes are more common if the neurovascular contact occurs at the transition zone or central myelin section, in particular when associated with nerve displacement and atrophy. ABBREVIATIONS:AICA ϭ anterior inferior cerebellar artery; CN ϭ cranial nerve; GN ϭ glossopharyngeal neuralgia; HFS ϭ hemifacial spasm; NVC ϭ neurovascular

show abstract

“…GPN occurs much less frequently than trigeminal neuralgia 1 ; the ratio between them varies from study to study, ranging from 5.9:1 to 100:1. [2][3][4] The annual incidence rate of GPN, according to a population-based study, 5 is about 0.7 per 100,000. Overall, there is a higher incidence of GPN in men in most series, but it never reached statistical significance.…”

mentioning

confidence: 99%

Glossopharyngeal Neuralgia

Slavin¹

2004

Seminars in Neurosurgery

View full text Add to dashboard Cite

Glossopharyngeal neuralgia (GPN) is a pain syndrome characterized by attacks of severe pain in the sensory distribution of the glossopharyngeal nerve. Most cases of GPN respond to treatment with carbamazepine and other anticonvulsants. The causative element of essential GPN appears to be a vascular compression of the glossopharyngeal nerve root and the upper rootlets of the vagus nerve; therefore, the most definitive surgical treatment consists of microvascular decompression of the ninth (and tenth) nerve in the posterior cranial fossa. In cases of secondary GPN and when microvascular decompression is not possible, intracranial rhizotomy of the glossopharyngeal and upper portion of the vagal nerve roots may be the next logical step in surgical management. Extracranial neurotomy and percutaneous radiofrequency rhizotomy are useful for patients with GPN who have failed medical treatment but for some reason cannot undergo intracranial intervention.

show abstract

Glossopharyngeal Neuralgia

Cited by 13 publications

References 0 publications

Glossopharyngeal neuralgia with syncope

Glossopharyngeal neuralgia with syncope

Imaging of Neurovascular Compression Syndromes: Trigeminal Neuralgia, Hemifacial Spasm, Vestibular Paroxysmia, and Glossopharyngeal Neuralgia

Glossopharyngeal Neuralgia

Contact Info

Product

Resources

About