Tinnitus

Tinnitus: Excerpt from The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter

Sara Lynn Neal

Tinnitus, which has been described as “ear noise,” consists of sounds heard by the patient with no sound source external to the head. Although infinite variations can occur, most commonly patients will describe ringing, buzzing, clicking, hissing, or humming. Of the population, 10% to 14% will complain of prolonged, recurrent tinnitus, with 20% of these people having symptoms that have a significant impact on their quality of life (1,2). In the United Kingdom, 7% of the population will at some time seek evaluation in primary care for tinnitus (2).

Approach

Tinnitus is not a disease, but an indication of some other ongoing process, pathologic or not. The first clues to diagnosing which process is responsible for the tinnitus are the type of sound heard and any relationship to the pulse or respiration. These clues subdivide tinnitus into two general categories, vibratory and nonvibratory.

A. Types of tinnitus

1. Vibratory (objective, pseudotinnitus). These sounds are often synchronous with the pulse. They are real sounds and mechanical in origin; they can sometimes be heard by the examiner as well as the patient who may describe the sound as pulsatile. Sources, either vascular or muscular, include:

a. Venous hum: caused by eddy currents in the jugular vein and exacerbated by concurrent conductive hearing loss.

 b. Arteriovenous malformations: most commonly between the occipital artery and the transverse sinus.

 c. Arterial bruits: most commonly from the petrous carotid system.

 d. Myoclonus of nearby structures, most commonly the palate, stapedius muscle, or tensor tympani. These are usually asynchronous with the pulse.

 e. A patulous or abnormally patent eustachian tube can cause chronic or intermittent tinnitus. Sometimes related to respirations, it is frequently described as a “hissing” sound.

 2. Nonvibratory (subjective). This type is more common. Subdivision into central versus peripheral tinnitus is helpful.

 a. Central tinnitus is caused by any eighth nerve or cortex lesion, including multiple sclerosis (MS).

 b. Peripheral tinnitus has many perpetrators including metabolic disorders (hyperlipidemia, thyroid disease, zinc deficiency), infection, medications (section II.E.), cerumen impaction, sensorineural hearing loss (especially presbycusis or noise-induced), Ménière’s disease, temporomandibular joint dysfunction, otosclerosis, and spontaneous cochlear emissions.

 B. Special concerns. Tinnitus can be a component of several conditions that threaten hearing such as Ménière’s disease, acoustic neuroma, or Cogan’s syndrome. Special attention should be paid to patients presenting with unilateral tinnitus, associated vertigo, unilateral sensorineural hearing loss, and eye inflammation.

History

Important features of the history should include:

A. Date of tinnitus onset, particularly any relation to an illness or change in drug regimen.

 B. A description of the tinnitus may help subdivide into vibratory and nonvibratory sources. Are there any exacerbating or ameliorating factors? An association with respirations or pulse points to a vibratory source. Positional change (such as lowering the head between the knees causing venous engorgement), variation with respirations, or distortion of one’s own voice can point toward a patulous eustachian tube as the mechanism for tinnitus.

 C. Fluctuation of symptoms. This is commonly associated with Ménière’s disease.

 D. History of noise exposure or hearing loss. Noise-induced hearing loss usually causes high-pitched tinnitus, whereas Ménière’s disease usually produces a lower-pitched sound. Conductive hearing loss from cerumen impaction, otitis media, or otosclerosis can heighten the awareness of internal vibratory sounds such as a venous hum or myoclonus. Presbycusis, or degeneration within the organ of Corti, is frequently seen in the elderly. It is associated with high-frequency hearing loss and high-pitched tinnitus (Chapter 6.2).

 E. Medication history. Drugs can be a major contributor to tinnitus (e.g., salicylates, caffeine, aminoglycosides, alcohol, quinidine, nonsteroidals, carbamazepine, levodopa, propranolol (Inderal), and aminophylline) (3). Some hormonal preparations have also been implicated as has the postpartum state.

 F. Significant weight loss can be associated with a patulous eustachian tube (Chapter 2.13).

G. Concurrent medical conditions to be considered include hypertension, diabetes mellitus, thyroid disorders, hyperlipidemia, and infection. Arteriovenous sounds will be heightened by increased cardiac output. Vascular disease can cause ischemia of the auditory organs, including the cortex. Neural impulses can be affected by diabetes or MS.

H. Psychiatric disturbances can affect sound perception. Ask about anxiety or depression, which can heighten awareness of internal auditory sounds. In turn, tinnitus can exacerbate these underlying conditions. Auditory hallucinations can be assessed by mental status testing.

I. Psychological effects. Ask about impact on sleep, concentration, hearing, memory, irritability, and sense of well-being.

Physical examination

 Focus on the head, ears, eyes, nose, throat, and neck as well as the cardiovascular and neurologic systems. Assess vital signs and perform a complete ear examination, including evaluation for obstruction of the external auditory canal. Look for tympanic membrane landmarks, tympanic pulsations, or signs of tumor. Auscultate the external auditory canal for transmitted sounds and use tuning forks to assess air and bone conduction. Observe the neck for thyroid masses and auscultate for thyroid or carotid bruits. Evaluate extraocular movements, speech discrimination, and the integrity of the central nervous system (gait, equilibrium, sensation). If appropriate, include evaluation of mood, affect, and perception (e.g., hallucinations).

Testing

A. Clinical laboratory tests. Most tinnitus patients will need only audiometry (4,5). If indicated by history and physical examination, consider thyroid functions, electrolytes, lipids, sedimentation rate, toxicology, syphilis serology, or rheumatology screen. A complete audiometric evaluation (pure tone and speech thresholds, speech discrimination, acoustic reflexes, and impedence testing) should always be done, especially to search for sensorineural hearing loss (4,5). A tympanogram may reveal pulsations coincident with the heart rhythm or respirations.

 B. Imaging. Plain radiographs are rarely useful. Evaluation for neoplasm, especially an acoustic neuroma, is best done with magnetic resonance imaging (MRI), which will also delineate eighth nerve lesions and cortex damage. Computed tomography (CT) with contrast is superior to MRI in suspected lesions of the temporal bone and mastoids (5). Auditory brainstem-evoked responses can help to localize cortical lesions or MS (1,5). Duplex ultrasound will reveal carotid stenosis. An angiogram may be necessary to examine vasculature near the inner ear. Patients with pulsatile tinnitus may need MRI, CT, and angiography before a definitive cause is found (5).

Diagnostic assessment

Because tinnitus is a symptom, not a disease, the focus of evaluation should be on identifying those few patients with serious or treatable causes and convincing the remaining patients of the nonthreatening nature of the symptom. The key to diagnosing tinnitus is determining if it is vibratory or nonvibratory. If vibratory, search for a structural source (e.g., vascular complex, muscular component, eustachian tube) of the sound through audiometry and imaging. Nonvibratory tinnitus, although more common, often has a less easily definable cause. Consider drug effects and hearing loss first, then search for altered metabolic states (e.g., diabetes, hyperthyroidism, or infection), not forgetting psychiatric causes. Evaluate for neurologic conditions (acoustic neuroma, damage to the organ of Corti or a brain lesion) as indicated.

References

1. Pfeifer KJ, Rosen GP, Rubin AM. Tinnitus: etiology and management. Clin Geriatr Med 1999;15:193–203.

2. Vesterager V. Fortnightly review: tinnitus—investigation and management. BMJ 1997;314:728–731.

3. Seligmann H, Podoshin L, Ben-David J, et al. Drug-induced tinnitus and other hearing disorders. Drug Saf 1996;14:198–212.

4. Seidman MD, Jacobson GP. Update on tinnitus. Otolaryngol Clin North Am 1996;
29:455–465.

5. Fortune DS, Haynes DS. Tinnitus—current evaluation and management. Med Clin North Am 1999;83:153–162.

Book Source Details

• Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
• Author(s): Robert B. Taylor (editor)
• Year of Publication: 2000
• Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter Authors: Robert B. Taylor (editor) Publisher: Lippincott Williams & Wilkins Copyright: 2000 ISBN: 0-78172-094-X

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