Do You Hear What I Hear: Tinnitus and Auditory Disturbances

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Historical Context – A Tale of Tuning Forks

The eighteenth century saw the invention of the tuning fork, a tool that, due to its remarkable simplicity and sound physics, has remained largely unchanged since its conception. The modern tuning fork originally arose as a musical instrument, invented by London trumpeter John Store (1-3). The understanding of its science, though, finds roots in the sixteenth century, when G Cardano, an Italian astrologer, physician, and mathematician, hypothesized that sound could be transmitted through bone as well as air, a concept that would be used only years later by a different physician, H Capivacci, to differentiate different kinds of hearing loss (1). This hypothesis was put to the test again nearly one hundred years later by G C Schelhammer, a German physician, who, in perhaps true emergency medicine fashion, made do with what tool he had – a simple table fork (2, 3).  Over the years, tuning forks fell quickly out of favor in the musical world, but its utility as a bedside tool a la Rinne and Weber are enough to reserve a spot in the B pod drawer.

Physiology of Hearing

The auricle or pinna of the ear helps capture sound waves, which then transmit through air to the tympanic membrane via the external acoustic canal. When sound waves make contact with the tympanic membrane, it vibrates, causing subsequent vibration of the “middle ear”. The middle ear is comprised of a series of three bones, also called the ossicles: the malleus, incus, and stapes. The ossicles further amplify the sound. The foot of the stapes contacts the oval window, and sound waves are then transmitted through the fluid-filled cochlea (4). This mechanical energy is then converted into electrical energy via hair cells. This electrical signal ultimately coalesces to propagate a signal to the cochlear portion of the vestibulocochlear nerve (cranial nerve VIII). The afferent nerve then meets its nucleus at the superior medulla and up into the auditory cortex (5, 6). The anterior inferior cerebellar artery (AICA) and its branches as well as the vertebral and basilar arteries supply blood to the vestibulocochlear nerve (7).

Pathophysiology

Hearing loss is classically described as sensorineural or conductive in nature. Broadly, conductive hearing loss can occur by any disruption in the transmission of sound waves via the pinna through the external acoustic canal, tympanic membrane, ossicles, round window, and cochlea. Sensorineural hearing loss occurs by any disruption of the mechanotransduction itself, in which sound waves are unable to be propagated as electrical signals to the auditory cortex (5, 6). Broadly speaking, sensorineural hearing loss is more likely to be associated with serious underlying pathology in the emergency department as compared to conductive hearing loss.

Tinnitus is most commonly idiopathic in nature but is most typically accompanied by some degree of associated hearing loss.  Although the majority of cases are not dangerous, it can be particularly distressing for patients and can affect quality of life. In fact, data from previous studies have found anywhere from twenty-six and seventy-seven percent of patients with tinnitus will manifest some kind of psychiatric comorbidity, particularly anxiety, depression, sleep disorders, and even suicidality. (9-11)

Though classically thought of as a “ringing” in the ear, patients may describe a variety of sounds, including rushing, buzzing, or hissing (9, 10). A variety of terms have been used to classify tinnitus based on the apparent origin of the sound. In the majority of cases, the annoying sound cannot be heard by anyone but the patient, which is called subjective tinnitus. Subjective tinnitus is sometimes also called neurophysiologic or sensorineural tinnitus, as the underlying pathology is thought to lie somewhere within the auditory nervous system, anywhere between the cochlea and auditory cortex. By contrast, objective tinnitus occurs when the sound described by the patient can actually be heard or otherwise observed by the examiner (9). This is also called somatic tinnitus, as it has an internal acoustic source (9, 10). These are further divided into pulsatile and non-pulsatile tinnitus. Pulsatile tinnitus pulses in synchrony with the patient’s heartbeat and is secondary to a vascular structure. Usually, this is a venous “hum” from normal venous flow and, while bothersome, is ultimately benign. Less commonly, pulsatile tinnitus is the result of arteriovenous malformations, glomus tumors, and carotid stenosis. Non-pulsatile tinnitus is a type of objective tinnitus that is nonvascular in origin. Examples include Eustachian tube dysfunction and middle ear muscle spasms such as those that occur in tensor tympani syndrome. (9, 10, 11-13)

Triage and Diagnostics

The majority of cases of hearing loss and tinnitus are not immediately dangerous and may be safely deferred to the outpatient setting. There are, however, several etiologies of such complaints that are dangerous and require prompt evaluation in the emergency department. The approach to hearing loss and/or tinnitus in the emergency department must focus on identifying characteristics that may clue the examiner in on a potentially harmful etiology. This begins, as always, with a targeted but thorough history. Important qualities of the complaint include the acuity of onset, laterality, and associated symptoms such as vertigo or vision changes. While the intensity and quality of tinnitus do not offer much insight, determining whether or not it is pulsatile is important.

More concerning features of hearing loss and tinnitus: (10, 14-16)

  • Acute onset, especially if bilateral sensorineural hearing loss

  • Recurrent unilateral hearing loss

  • Abnormal neurologic exam

  • Pulsatile tinnitus

While specialty equipment found in an otolaryngologist’s office may not be readily available, crucial information can still be ascertained by physical exam in the emergency department. The external pinna, adjacent skin, and face should be carefully examined for any lesions to suggest viral infection such as herpes zoster, though this more commonly causes hyperacusis (12). An otoscope should be used to inspect the external acoustic meatus, internal acoustic meatus, and tympanic membrane for any foreign body, impacted cerumen, or torn tympanic membrane (6). Every patient presenting with hearing loss or tinnitus should undergo a thorough neurologic exam, as any abnormal neurologic exam finding may indicate a central cause of presenting symptoms (6, 10, 14, 15). Although not widely performed in the ED, the Weber and Rinne tests can help distinguish conductive versus sensorineural hearing loss, an important distinction as sudden sensorineural hearing loss is more likely to have serious underlying pathology (6, 8, 14). If a tuning fork is unavailable, the emergency physician may instead perform a simple humming test in a patient with unilateral hearing loss. The patient hums, and if the patient hears this loudest in the affected ear, this indicates conductive hearing loss. The humming test has been shown to be greater than 90% sensitive in detection of conductive versus sensorineural hearing loss in small studies and may be a potential alternative if needed (17).

Imaging has a role in the diagnostic evaluation of hearing loss and tinnitus with concerning features as outlined above. CT is specifically recommended against by the American Academy of Otolaryngology in causes of suspected sensorineural hearing loss. They instead recommend MRI, which can be deferred to outpatient if no high-risk features exist (18). In the event of a high-risk patient in the emergent setting, though, MRI is often not prompt enough and so a CT is often used instead (9). This is the favored approach to any patient with so-called “red flags” in most emergency medicine literature, as the diagnostic approach is necessarily different in the ED. Vessel imaging may be considered for pulsatile tinnitus or if concern for posterior CVA.

Lab tests are recommended only on a case-by-case basis when more systemic pathology is suspected (8).

Therapeutics

            Unfortunately, the options for the treatment of hearing loss and/or tinnitus, while variable based on etiology, remain rather limited. In the case of conductive hearing loss, ED treatment aims at direct visualization and subsequent removal of any visible blockage, when possible. In the case of sensorineural hearing loss, when acutely dangerous causes have been ruled out, patients may be assured that some degree of spontaneous recovery is common, though the likelihood is affected by severity, age, and cardiovascular comorbidity (10). Even in the case of a confirmed viral infection, there is no role for antivirals. The only pharmacologic intervention shown to offer any potential benefit is steroids, at a dose of 1 mg/kg/d prednisone for 7-14 days (8, 10). While the data is mixed, steroids seem to improve speed of recovery for a wide variety of sensorineural hearing loss. Patients should be provided reassurance and counseled to avoid ototoxic medications. (10)

References

  1. Bickerton, B. and Barr, G. “The origin of the tuning fork”. 1987. Journal of the Royal Society of Medicine. 80: 771-773

  2. Pearce JMS. “Early days of the tuning fork.” 1998. Journal of Neurology, Neurosurgery & Psychiatry. 65: 728

  3. Feldmann, H. “History of the tuning fork. II: Evolution of the classical experiments by Weber, Rinne and Schwabach”. 1997. Laryngorhinootologie. 76: 318-326

  4. Kong, E. and Fowler, J. “Rinne Test”. 2022. Treasure Island, StatPearls Publishing. Available from: https://www.ncbi.nlm.nih.gov/books/NBK431071/

  5. Isaacson, J. and Vora, N. “Differential Diagnosis and Treatment of Hearing Loss”. 2003. Am Fam Physician.68: 1125-1132

  6. Lalwani A.K. (2014). Disorders of hearing. Kasper D, & Fauci A, & Hauser S, & Longo D, & Jameson J, & Loscalzo J(Eds.), Harrison's Principles of Internal Medicine, 19e. McGraw Hill. https://accessmedicine.mhmedical.com/Content.aspx?bookid=1130&sectionid=79725558

  7. Barral, J.; Croibier, A. “Vestibulocochlear nerve”. 2009. Manual Therapy for the Cranial Nerves. Pages 167-180

  8. Cheng, A.; Mitchell, Z.; Foote, J. “Can you hear me?” 2014. Can Fam Physician. 60: 907-909

  9. Welsh, K.; Nath, A.; Lewin, M. “Evaluation of Tinnitus in the Emergency Department”. 2011. Up to Date on Tinnitus. Available from: https://www.intechopen.com/chapters/25108

  10. Henry, J.; Zaugg, T.; Myers, P.; Kendall, C.; Michaelides, E. “A triage guide for tinnitus”. 2010. The Journal of Family Practice. 59: 389-393.

  11. Altissimi, G. et al. “When alarm bells ring: emergency tinnitus”. 2016. European Review for Medical and Pharmacological Sciences. 20: 2955-2973.

  12. Westcott, M.; Sanchez, T.; Diges, I.; Saba, C.; Dineen, R.; McNeill, C.; Chiam, A.; O’Keefe, M.; Sharples, T. “Tonic tensor tympani syndrome in tinnitus and hyperacusis patients: a multi-clinic prevalence study”. 2013. Noise Health. 15: 117-128

  13. Keidar, E.; De Jong, R.; Kwartowitz, G. “Tensor Tympani Syndrome”. 2022. StatPearls. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519055

  14. Esmaili, A. and Renton, J. “A review of tinnitus”. 2018. Australian Journal of General Practice. 47: 205-208

  15. Wu, V.; Cooke, B.; Eitutis, S.; Simpson, M.; Beyea, J. “Approach to tinnitus management”. 2018. Can Fam Physician. 64: 491-495

  16. Carter, S. and Laird, C. “10 Assessment and care of ENT problems”. 2005. Emerg Med J. 22: 128-139.

  17. Ahmed, O.; Gallant, S.; Ruiz, R.; Wang, B.; Shapiro, W.; Voigt, E. “Validity of the Hum Test, a Simple and Reliable Alternative to the Weber Test”. 2018. Ann Otol Rhinol Laryngol. 127: 402-405

  18. Chandrasekhar, S.; Tsai Do, B.; Schwartz, S. “Clinical Practice Guideline: Sudden Hearing Loss (Update)”. 2019. American Academy of Otolaryngology – Head and Neck Surgery. 161: S1-S45

Authorship

Written by Megan Wright, PGY-1, University of Cincinnati Department of Emergency Medicine

Review and Posting by Jeffery Hill, MD MEd, Associate Professor, University of Cincinnati Department of Emergency Medicine