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Herpes Zoster of the Larynx

John M. Carter, MD1; David Cai, BS1; Brian A. Moore, MD, FACS2 1Tulane University School of Medicine, 2Ochsner Clinic Foundation

Introduction Discussion Discussion

Figure 1 . Flexible fiberoptic laryngoscopy demonstrating vesicular lesions of the hemilarynx, a

paralyzed right vocal fold and pooling of secretions.

Abstract

Varicella Zoster is a systemic

disease process that rarely

occurs in the larynx. A 97

year old gentleman

encountered in the clinic and

then the hospital setting

presented with severe

dysphagia, odynophagia and

hoarseness. This case report

includes endoscopic images

of the larynx that reveal

mucosal vesicles of the

hemilarynx, pooling of

secretions and a unilateral

vocal cord paralysis. Varicella

zoster antibody titers for IGG

were positive. The gentleman

improved with systemic

antiviral medication, with

marked improvement of both

subjective and objective

findings.

Herpes zoster of the larynx may present in a variety of

ways. The patient may have one or more cranial nerve

palsies, painful mucosal vesicles, or pain without visible

herpetic lesions. Cranial nerves IX, X, and XI are most

often involved but CN VII and VIII may be affected in

more extensive cases.1 Patients may or may not have

concurrent skin involvement.

Varicella zoster in the head and neck affects various

cranial nerves in a locoregional distribution. The larynx

is supplied by the vagus nerve, namely the superior

laryngeal and recurrent laryngeal nerves. The superior

laryngeal nerve provides sensory innervation to the

supraglottic structures and vocal folds through its

internal branch, while the external branch provides

motor innervation to the cricothyroid muscle. The

recurrent laryngeal nerve innervates the remainder of

the motor function of the laryngeal muscles and sensory

innervation for the subglottis.7

Mucosal lesions of zoster of the head and neck are not

typically limited to one nerve distribution and do not

necessarily stem from one ganglion.1,2 In our case

disease was confined to the distribution of the superior

and recurrent branches of cranial nerve X. Lin et al.

described the only 11 previously reported cases of

varicella zoster infection that presented as cranial nerve

palsies with mucosal lesions that lacked skin

manifestations or evidence of herpes zoster oticus.

Four of these cases involved only the hemilarynx and

cranial nerve X, as in our presentation.1

Laboratory testing is supplemental to clinical

presentation and endoscopic findings. Useful tests

are varicella antibodies (IGM and IGG) and PCR

testing for viral genome detection. IGG may appear

as soon as 4 days after mucosal lesions, whereas

IGM typically rises 8-10 days afterwards.1,9 The

patient in this case was seropositive for varicella

antibody IGG, while IGM antibodies were negative.

It has been shown that not all cases present with a

positive IGM. The sensitivity of serum antibody IGM

ranges from 50-84%.1,6 A two-fold increase in IGG

has also been shown to be more useful in the

detection of herpes zoster reactivation than IGM.8

When the diagnosis in question, PCR has been

shown to have a sensitivity that approaches 100%.5

However, obtaining a bedside cotton swab for PCR

diagnosis may not be easily achievable or

comfortable for the patient.

Evidence for the treatment of these lesions is

lacking and largely based on treatment of herpes

zoster oticus. Despite definitive evidence, one can

justify attempting medical therapy with anti-viral

medications and steroids with the intention of

hastening the course of vesicle resolution and

perhaps return of nerve function.9 As in this case,

supportive measures such as gastrostomy tubes

may be required.

Herpes zoster is a rare but uncommon cause of

neuropathy in the head and neck and should be

considered whenever vesicular mucosal lesions are

present. Diagnosis is largely established through

clinical exam and confirmed through laboratory

testing. Treatment with anti-viral medications and

steroids lacks convincing evidence but may be used

to hasten recovery.

Varicella Zoster is a common systemic disease that

rarely affects the larynx.1-4 The virus is known to

establish a latent infection in the spinal cord or

cranial nerve ganglia that reactivates secondary to

various stressors. It has often been described in

head and neck as Ramsay Hunt Syndrome type II,

stemming from the geniculate ganglion. Patients

suffering from herpes zoster present with vesicular

eruptions, acute pain and nerve paralysis in the

distribution of the affected nerves. Herpes zoster of

the larynx is uncommon and often presents with

multiple cranial neuropathies.1-3 Furthermore, its

vesicular appearance may be confused with a

laryngeal neoplasm.

Herpes zoster of the larynx may manifest with

unilateral vocal fold paralysis, mucosal vesicles of

the hemilarynx, dysphagia and odynophagia. The

diagnosis of this disease process is largely clinical

and may be supplemented by viral antibody assays

and polymerase chain reaction (PCR).1,3,5,6

1. Lin YY. Kao CH. Wang CH. Varicella zoster virus infection of the pharynx

and larynx with multiple cranial neuropathies. Laryngoscope 2011;121:1627-

30.

2. Pinto JA, Pinto HC, Ramalho Jda R. Laryngeal herpes: a case report. J

Voice 2002;16:560–563.

3. Chitose S-I, Umeno H, Hamakawa S, Nakashima T, Shoji H. Unilateral

associated laryngeal paralysis due to varicella-zoster virus: virus antibody

testing and videofluoroscopic findings. J Laryngol Otol 2008;122:170-6.

4. Watelet JB, Evrard AS, Lawson G, et al. Herpes zoster laryngitis: case

report and serological profile. Eur Arch Otorhinolaryngol 2007;264:505–7.

5. Beards G, Graham C, Pillay D. Investigation of vesicular rashes for HSV

and VZV by PCR. J Med Virol 1998;54(3):155-7.

6. Van Loon AM, van der Logt JT, Heessen FW, Heeren MC, Zoll J. Antibody-

capture enzyme-linked immunosorbent assays that use enzymelabelled

antigen for detection of virus-specific immunoglobulin M, A and G in patients

with varicella or herpes zoster. Epidemiol Infect 1992;108:165–174.

7. Yoshida Y, Tanaka Y, Hirano M, Nakashima T. Sensory innervation of the

pharynx and larynx. Am J Med 2000;108:51S–61S.

8. Kawaguchi K. Inamura H. Abe Y. Koshu H. Takashita E. Muraki Y.

Matsuzaki Y. Nishimura H. Ishikawa H. Fukao A. Hongo S. Aoyagi M.

Reactivation of herpes simplex virus type 1 and varicella-zoster virus and

therapeutic effects of combination therapy with prednisolone and valacyclovir

in patients with Bell's palsy. Laryngoscope 2007;117:147-56.

9. Uscategui T. Doree C. Chamberlain IJ. Burton MJ. Antiviral therapy for

Ramsay Hunt Syndrome (herpes zoster oticus with facial palsy) in adults

Cochrane Database Syst Rev. 2008 Oct 8;(4):CD006851.

Conclusions

References

John M. Carter, MD

Tulane University School of Medicine

Email: jcarter9@tulane.edu

Phone: 504-988-5454

Contact

Figure 2. Flexible fiberoptic laryngoscopy

demonstrating complete resolution of lesions.

A 97 year old male presented with one week of

worsening dysphagia, odynophagia and a mild

hoarseness. The patient was still able to tolerate a

normal diet. During flexible fiberoptic laryngoscopy

the patient did not have a vocal fold paralysis but

did have a small ulcer of the right aryepiglottic fold.

Two days later his dysphagia worsened and he was

no longer able to tolerate liquids.

Esophagogastroduodenoscopy was performed and

the only abnormality was a Schatzski ring at the

gastroesophageal junction. Secondary to his

severe dysphagia and a modified barium swallow

study that showed aspiration and hypopharyngeal

pooling of contrast, a gastrostomy tube was placed.

Contrast enhanced computed tomography of the

neck did not reveal any abnormality. The following

day flexible fiberoptic laryngoscopy was repeated,

revealing ulcerations of the right hemilarynx, pooling

of secretions and a complete right vocal fold

paralysis (Figure 1). The left hemilarynx was

unaffected. Laboratory testing was significant for

Varicella zoster IGG antibody titers that were five

times normal limits, 5.06 (NL= 0.0-0.9). Varicella

IGM antibody testing was negative.

The patient was started on intravenous valacyclovir

and prednisone. The following day his subjective

dysphagia began to improve. Laryngoscopy

revealed a reduction in the quality of the erythema

and ulcerations. Finally, two weeks after treatment,

the patient had a complete resolution of the vesicles

(Figure 2). The previously paralyzed right cord

demonstrated improved, but not yet normal mobility.

Case Presentation