Case Report Amantadine-Induced Patulous Eustachian Tubes

Hindawi Publishing CorporationCase Reports in OtolaryngologyVolume 2013, Article ID 426413, 2 pageshttp://dx.doi.org/10.1155/2013/426413

Case ReportAmantadine-Induced Patulous Eustachian Tubes inParkinson’s Disease

J. T. Boyd1 and D. A. Silverman2

1 Department of Neurological Sciences, College of Medicine, University of Vermont, UHC-Arnold 2, 1 South Prospect Street,Burlington, VT 05401, USA

2Department of Surgery (Otolaryngology), College of Medicine, University of Vermont, Burlington, VT 05401, USA

Correspondence should be addressed to J. T. Boyd; james.boyd@vtmednet.org

Received 3 September 2013; Accepted 10 October 2013

Academic Editors: T. Hillman and Y. Orita

Copyright © 2013 J. T. Boyd and D. A. Silverman. This is an open access article distributed under the Creative CommonsAttribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work isproperly cited.

Patulous Eustachian tube (PET) is a common condition that produces symptoms of aural fullness and autophony. We describe aParkinson’s disease (PD) patient that experienced a reversible bilateral patulous (hyperpatent) Eustachian tube syndrome inducedby treatment with amantadine hydrochloride. The clinical features, relevant anatomy and physiology, and associated risk factorsfor PET are reviewed.

1. Introduction

Patulous Eustachian tube (PET) is a common conditionthat presents with the primary complaint of distorted orechoed autophony. Autophony is the amplified auditoryperception of self-generated sounds such as respiration,vocalization, and swallowing [1–3]. Additional presentingfeatures can include a feeling of aural fullness, mild vertigo orimbalance, recurrent nasal sniffing to relieve autophony, andpositional symptom improvement when supine. Persistentcommunication of the pharynx and middle ear occurs inthe setting of impaired closure of the Eustachian tube at thenasopharyngeal orifice [4, 5]. Previously reported contribut-ing factors include weight loss, caffeine use, pregnancy, andmedications including diuretics and nasal decongestants [3–7]. Neurological disorders that have been associatedwith PETinclude motor neuron disease, multiple sclerosis, and stroke[3–8].

In healthy cases, the ET closes passively via recoil ofthe elastin hinge and force generated by the deformationof Ostmann’s fat pad. Opening occurs during yawning,sneezing, and deglutition actively by contraction of the tensorveli palatini and passively by the levator veli palatini. Mucusproducing goblet cells line the medial two-thirds of the ETnear the pharyngeal orifice [3, 7].

2. Case Presentation

We report the case of a patient who developed PET inducedby amantadine hydrochloride which resolved with discon-tinuation. The patient is a 50-year-old man with a one-yearhistory of Parkinson’s disease (Hoehn and Yahr stage 1).

Amantadine hydrochloride was initiated and escalated to100mg twice daily with improvement of parkinsonism andinitial absence of adverse effects. Approximately four weeksafter initiation of amantadine, the patient presented withcomplaints of oropharyngeal dryness with constant left andintermittent right autophony. Visualization of the tympanicmembrane revealed left-sided mobility in association withdeep respiration, supporting a diagnosis of Eustachian tubehyperpatency. No additional pathology was identified onflexible laryngoscopic examination.

Discontinuation of amantadine resulted in a resolution ofsymptoms over seven days. Amantadine rechallenge resultedin a rapid reemergence of the aforementioned symptoms.Thepatient elected to undergo unilateral left tube myringotomywith limited symptom relief.

3. Discussion

Reversible patulous Eustachian tubes were induced by aman-tadine in our patient. PET is described in the literature as

2 Case Reports in Otolaryngology

common and often induced by medications, though peer-reviewed reports of particular medication-induced PET arelacking. PET has not previously been reported in associ-ation with Parkinson’s disease or its treatment. Amanta-dine is a commonly used symptomatic treatment in bothearly and advanced PD. Multiple mechanisms of actionare proposed including NMDA glutamate antagonism andenhanced release/reduced reuptake of dopamine [9]. Drymouth, constipation, and other peripheral anticholinergicside effects are commonly encountered with amantadine.Previous investigations suggest that these may be related toa reduced cholinergic release rather than receptor antag-onism [9]. Other medications previously associated withPET include diuretics and decongestants [4, 5]. Given thesimultaneous complaints of oral dryness and known anti-cholinergic side effects, amantadinemay have reducedmucusproduction/increased viscosity to promote PET. Weight loss,altered voluntary and involuntary muscle activation, andmucosal dryness are common to both PET and PD. Thus,the recognition of a potential association between PET andamantadine represents an important clinical observation.

References

[1] G. E. Shambaugh, “Continuously open eustachian tube,”Archives of Otolaryngology, vol. 27, no. 4, pp. 420–425, 1938.

[2] A. F. O’Connor and J. J. Shea, “Autophony and the patulouseustachian tube,” Laryngoscope, vol. 91, no. 9 I, pp. 1427–1435,1981.

[3] R. C. O’Reilly and I. Sando, “Anatomy and physiology of theeustachian tube,” inCummings Otolaryngology—Head andNeckSurgery, P.W. Flint, B. H. Haughey, V. J. Lund et al., Eds., Mosby,Philadelphia, Pa, USA, 3rd edition, 2010.

[4] J. F. Grimmer and D. S. Poe, “Update on eustachian tubedysfunction and the patulous eustachian tube,”Current Opinionin Otolaryngology and Head and Neck Surgery, vol. 13, no. 5, pp.277–282, 2005.

[5] R. K. Dyer Jr. and J. T. McElveen Jr., “The patulous eustachiantube: management options,” Otolaryngology—Head and NeckSurgery, vol. 105, no. 6, pp. 832–835, 1991.

[6] E. Cunsulo et al., “Functional anatomy of the ET,” InternationalJournal of Immunopathology and Pharmacology, vol. 23, no. 1,supplement, pp. 4–7, 2010.

[7] R. F. Canalis and P. R. Lambert, “Anatomy and embryology ofthe auditory and vestibular systems,” inTheEar: ComprehensiveOtology, R. F. Canalis and P. R. Lambert, Eds., LippincottWilliams &Wilkins, Philadelphia, Pa, USA, 2000.

[8] K. Schellenberg, R. Bedlack, and D. Tucci, “Roaring in theears: patulous eustachian tube in bulbar amyotrophic lateralsclerosis,” Amyotrophic Lateral Sclerosis, vol. 11, no. 4, pp. 395–396, 2010.

[9] J. C. Stoof, J. Booij, B. Drukarch, and E. C. Wolters, “Theanti-parkinsonian drug amantadine inhibits the N-methyl-D-aspartic acid-evoked release of acetylcholine from rat neostria-tum in a non-competitive way,” European Journal of Pharmacol-ogy, vol. 213, no. 3, pp. 439–443, 1992.

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