Tinnitus is defined as the perception of sound in the absence of an external sound source. It may consist of single or multiple tones and may be described as high pitched, low pitched, buzzing, roaring, clicking, hissing, pulsatile, or continuous. Because tinnitus is a symptom rather than a disease and its pathogenesis remains uncertain, treatment is empiric and achieves variable levels of success. Given our current understanding, however, considerable control of this symptom is available. More than 36 million people in the United States report tinnitus, and about 8 million have a severe form of it. Tinnitus is most prevalent between the ages of 40 and 70 years and occurs equally among men and women.

Objective tinnitus is sound audible to both patient and physician; subjective tinnitus is heard only by the patient. Objective tinnitus may be found by an examiner during auscultation of the auditory canal or surrounding structures with a stethoscope. This form of tinnitus can be pulsatile, humming, roaring, clicking, or crackling. Associated conditions include vascular abnormalities, eustachian tube problems, tympanic muscle disorders, and central nervous system malformations (Table 10-1).

Subjective tinnitus is much more common than objective tinnitus and its cause remains largely speculative. Abnormalities in the cochlea, cochlear nerve, ascending auditory pathway, or auditory cortex may lead to subjective tinnitus. Studies suggest that cochlear hair cells injured by noise or head trauma may discharge repetitively, stimulating nerve fibers to discharge synchronously in such a manner that the central auditory system cannot differentiate the sensation from actual sound. Cochlear damage from chemical, physical, or vascular causes may reduce the suppressive influence of the central nervous system, enabling increased neuronal activity higher in the auditory system. Reduction of central inhibition at the level of the inferior colliculus (where auditory and nonauditory functions are thought to converge) caused by hearing loss or aging may result in central tinnitus. Given that sectioning the eighth cranial nerve has failed to eliminate subjective tinnitus, central mechanisms involving both auditory and nonauditory pathways at multiple levels are probably at work. Predispositions to subjective tinnitus include otologic, cardiovascular, metabolic, neurologic, pharmacologic, dental, and psychologic factors (Table 10-1).

Otologic conditions that produce tinnitus range in seriousness from benign cerumen impaction to tumors of the cerebellopontine angle. Occlusive conditions of the ear canal, including bony exostoses, external otitis, or foreign bodies, may be responsible. Middle ear disorders such as otitis media, otosclerosis, or a vascular tumor such as tympanic paraganglioma must be evaluated because these may be the sole cause of tinnitus. Inner ear problems, which include presbycusis, acoustic trauma, Meniere’s syndrome,
diseases of the central nervous system, hypercoagulability states, and acoustic neuroma (vestibular schwannoma), must be assessed with audiometric and appropriate site-of-lesion testing. The majority of patients with tinnitus have a history of noise exposure or presbycusis. A 30+ dB hearing loss from 3 to 8 kHz is the single most consistent finding among patients with tinnitus.

Cardiovascular factors associated with tinnitus include hypertension, anemia (tinnitus due to increased cardiac output), and arteriosclerosis (manifesting with pulsatile tinnitus). Metabolic conditions range from hyperthyroidism (also with increased cardiac output) and uncontrolled diabetes mellitus to triglyceridemia and vitamin A or B deficiency. A small percentage of patients report that tinnitus has resulted from trauma. Whiplash injuries with delayed tinnitus, closed head injuries, and basilar skull fractures may mark the onset of subjective tinnitus.