Glossopharyngeal neuralgia secondary to vascular compression in a patient with multiple sclerosis: a case report

Gaitour, Emil; Nick, Saeed Talebzadeh; Roberts, Charles; Gonzalez‐Toledo, Eduardo; Munjampalli, Sai; Minagar, Alireza; Vrooman, Bruce; Souzdalnitski, Dmitri; Zamnifekri, Behrouz

doi:10.1186/1752-1947-6-213

Cited by 8 publications

(8 citation statements)

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“…The diagnosis is confirmed by demonstration of VZV-DNA or VZV-antibodies in the CSF [8,9]. If there is unilateral herpes zoster infection of the larynx, insilateral LCN may be affected [10].…”

Section: Discussionmentioning

confidence: 99%

The Importance of Rehabilitation of Varicella Zoster Virus Neuropathy with Dysphagia: A Case Report and Literature Review

Nagai¹,

Ito²,

Nishizaka³

et al. 2017

Int J Phys Med Rehabil

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Dysphagia due to the varicella zoster virus (VZV) infection has the type of the main constituent Hunt syndrome and dysphagia of the main constituent a facial paralysis. The difference is considered to be the thing due to the ganglionic site which a virus reactivated. We report a case of the rehabilitation for dysphagia due to the VZV viral infection. Keywords: Rehabilitation; Varicella zoster virus; Dysphagia Case ReportA 76-year-old-female patient came to a nearby hospital with a sore throat and hoarseness in August, 2016. In acknowledgement of laryngeal edema, she was admitted to other hospital and did tracheotomy. There was the remaining, but the remaining was able to be eliminated by adding deglutition in the videofluorography at admission.VZV IgG rose by a blood test, and VZV virus neuropathy with dysphagia was diagnosed. She was admitted to the hospital for rehabilitation 65 days later. The Barthel index (BI) was 80 point and she had diabetes, hypertension, a gastric ulcer, but the control was good. The soft palate and lingual were normal. Left vocal cord paralysis was detected in swallowing videoendoscopy (VE) at admission, and the left vocal cord was fixed in a cadaveric position (Figure 1). Also, a larynx had remaining swallowing videofluorography (VF), but the remaining removal was possible in additional deglutition and compensation movement (Figure 2).There was a larynx invasion and a diet was paste foods and ate in 60 degrees reclining position, cervical rotation rank. The rehabilitation program trained her for dysphagia directly and conducted muscular strength reinforcement for muscle weakness. The diet was ingested by tube feeding two weeks before she was admitted, and she continued a paste meal after admission. There was not the aspiration in 90 degrees She removed a cannula 109 days after the onset, and became calm and finally became able to almost take in general diet with nothing. The ADL became independent, and the FIM became 126 points and became the home discharge 131 days after the onset. In VE at discharge, pharyngeal paralysis was improved and there was not the velopharyngeal insufficiency (Figures 3 and 4). Figure 4: There was the remaining, but the larynx movement was improved in the videofluorography at discharge. International Journal of PhysicalMedicine & Rehabilitation Nagai et al., Int J Phys Med Rehabil 2017, 5:In VF at discharge, a larynx had the remaining, but the movement was improved. Because a little larynx invasion was found when we consumed water, we taught it to drink by small quantity. DiscussionThe cause of the mixed laryngeal nerve paralysis is vascular and is neoplastic, and there is postoperative infectivity. The reports of the viral mixed laryngeal nerve paralysis increased [1][2][3][4][5][6][7].The diagnosis is confirmed by demonstration of VZV-DNA or VZV-antibodies in the CSF [8,9]. If there is unilateral herpes zoster infection of the larynx, insilateral LCN may be affected [10]. Our case had a diagnosis in VZV antibody in the CSF similarly.As for the tr...

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Section: Discussionmentioning

confidence: 99%

The Importance of Rehabilitation of Varicella Zoster Virus Neuropathy with Dysphagia: A Case Report and Literature Review

Nagai¹,

Ito²,

Nishizaka³

et al. 2017

Int J Phys Med Rehabil

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“…Pain may be triggered by contact of the tongue with the teeth[ 12 ] or with the back of the tongue. [ 13 ] Glossopharyngeal neuralgia may be associated with syncope (fainting) in 10% of the cases due to reflex bradycardia (efferent limb of reflex via vagal nerve) or occasionally induced by swallowing. Glossopharyngeal neuralgia is most frequently primary (compression of the nerve by adjacent vessel loop)[ 14 ] or secondary to an intrinsic brain lesion such as in multiple sclerosis[ 13 15 ] or in the Eagle-syndrome.…”

Section: Symptoms Of Lower Cranial Nerve Lesionsmentioning

confidence: 99%

“…[ 13 ] Glossopharyngeal neuralgia may be associated with syncope (fainting) in 10% of the cases due to reflex bradycardia (efferent limb of reflex via vagal nerve) or occasionally induced by swallowing. Glossopharyngeal neuralgia is most frequently primary (compression of the nerve by adjacent vessel loop)[ 14 ] or secondary to an intrinsic brain lesion such as in multiple sclerosis[ 13 15 ] or in the Eagle-syndrome. [ 16 ] Neuralgia of the laryngeal nerve is a rare condition and may be due to a deviated hyoid bone,[ 17 ] due to previous acute laryngitis,[ 18 ] a pharyngeal diverticulum,[ 19 ] or idiopathic.…”

Section: Symptoms Of Lower Cranial Nerve Lesionsmentioning

confidence: 99%

“…[ 77 78 ] Jugular-foramen-syndrome is characterized by acute onset dysphagia, dysphonia, and accompanied or preceded by cranial, cervical, or pharyngeal pain. [ 13 ] The most frequent cause of Jugular-foramen-syndrome is herpes zoster oticus with herpetic eruptions of the skin or the mucosa. MRI may reveal contrast enhancement around the jugular foramen, suggesting inflammation of the glossopharyngeal or vagal nerve ganglia.…”

Section: Disorders Of Lower Cranial Nervesmentioning

confidence: 99%

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Disorders of the lower cranial nerves

Finsterer

Grisold

2015

Journal of Neurosciences in Rural Practice

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Lesions of the lower cranial nerves (LCN) are due to numerous causes, which need to be differentiated to optimize management and outcome. This review aims at summarizing and discussing diseases affecting LCN. Review of publications dealing with disorders of the LCN in humans. Affection of multiple LCN is much more frequent than the affection of a single LCN. LCN may be affected solely or together with more proximal cranial nerves, with central nervous system disease, or with nonneurological disorders. LCN lesions have to be suspected if there are typical symptoms or signs attributable to a LCN. Causes of LCN lesions can be classified as genetic, vascular, traumatic, iatrogenic, infectious, immunologic, metabolic, nutritional, degenerative, or neoplastic. Treatment of LCN lesions depends on the underlying cause. An effective treatment is available in the majority of the cases, but a prerequisite for complete recovery is the prompt and correct diagnosis. LCN lesions need to be considered in case of disturbed speech, swallowing, coughing, deglutition, sensory functions, taste, or autonomic functions, neuralgic pain, dysphagia, head, pharyngeal, or neck pain, cardiac or gastrointestinal compromise, or weakness of the trapezius, sternocleidomastoid, or the tongue muscles. To correctly assess manifestations of LCN lesions, precise knowledge of the anatomy and physiology of the area is required.

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“…Le REZ est situé à 2 à 6 mm en aval de l'origine apparente pour le V, pour le VII à une distance inférieure à 3 mm de son origine apparente (loin du porus) et à 6 à 15 mm pour le VIII (près du porus) [3, 12,13]. Pour le glossopharyngien le REZ est près de la fossette supra olivaire du bulbe [5,6]. Pour le III nous n'avons pas retrouvé de donnée de la littérature sur son REZ.…”

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