Tinnitus may result from impacted cerumen, perforation of the tympanic membrane, or fluid in the middle ear, all of which “lead” to tinnitus due to the associated conductive hearing loss. The sensation is commonly described as low pitched, intermittent, and accompanied by muffled hearing and a change in the sound of one’s voice. In otosclerosis, tinnitus is constant but may disappear as the disease progresses. Acute otitis media sometimes produces a pulsating type of tinnitus that resolves as inflammation subsides. Pulsatile tinnitus is also associated with glomus tumors and posttraumatic arteriovenous fistulas.

Presbycusis, noise-induced hearing loss, and acoustic trauma can give rise to a high-pitched tinnitus that subjectively matches the frequency of greatest hearing loss. Transient tinnitus that follows acute noise exposure is a forerunner of hearing loss and a warning sign to avoid repeated exposure. Ototoxic drugs, such as the aminoglycoside antibiotics, may produce high-pitched tinnitus and hearing loss that often persist after the cessation of drug use. Salicylates are frequently responsible for reversible, dose-related tinnitus. Ménière disease results in transient, lowpitched tinnitus that varies with the intensity of the condition’s other symptoms, often worsening when vertigo and hearing loss are imminent. An acoustic neuroma produces a similar set of symptoms, but usually, the clinical course is progressive, with unilateral or asymmetric tinnitus frequently preceding other symptoms, such as vertigo (see Chapter 166). A sudden onset of severe unilateral tinnitus may be the first presenting symptom of sudden sensorineural hearing loss, which requires immediate medical attention.

When ambient noise is reduced, all people will notice some head sounds. These may stem from a variety of events, ranging from the rushing of blood (most severe in aortic insufficiency) to the contraction of auditory muscles. A loss of hearing due to conductive defects may accentuate the perception of tinnitus. Tinnitus cerebri is described as a roaring in the head and is believed to be vascular or neurologic in origin. A cerebral aneurysm with an audible bruit, a jugular megabulb anomaly, a palatal myoclonus with audible muscle contraction, and an unusually patent eustachian tube that transmits respiratory sounds are examples of “objective” tinnitus in which the sounds can be heard by the examiner. Tinnitus may also be associated with temporomandibular joint dysfunction (Costen syndrome). In rare cases, intermittent tinnitus may be caused by a spasm or flutter of the tensor tympani or stapedius muscles of the middle ear.

Depressed and neurotic individuals may have less tolerance for normal head sounds and complain of them when in quiet settings. The ability to accommodate tinnitus is also subject to much individual variation. Tolerance is lessened by fatigue and emotional stress.