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Tinnitus is a noise in the ears. It is experienced by 10 to 15% of the population.
Subjective tinnitus is perception of sound in the absence of an acoustic stimulus and is heard only by the patient. Most tinnitus is subjective.
Objective tinnitus is uncommon and results from noise generated by structures near the ear. Sometimes the tinnitus is loud enough to be heard by the examiner.
Tinnitus may be described as buzzing, ringing, roaring, whistling, or hissing and is sometimes variable and complex. Objective tinnitus typically is pulsatile (synchronous with the heartbeat) or intermittent. Tinnitus is most noticeable in quiet environments and in the absence of distracting stimuli and, thus, frequently seems worse at bedtime.
Tinnitus may be intermittent or continuous. Continuous tinnitus is at best annoying and is often quite distressing. Some patients adapt to its presence better than others; depression occasionally results. Stress generally exacerbates tinnitus.
Subjective tinnitus is thought to be caused by abnormal neuronal activity in the auditory cortex. This activity results when input from the auditory pathway (cochlea, auditory nerve, brain stem nuclei, auditory cortex) is disrupted or altered in some manner. This disruption may cause loss of suppression of intrinsic cortical activity and perhaps creation of new neural connections. Some believe the phenomenon is similar to the development of phantom limb pain after amputation. Conductive hearing loss (eg, caused by cerumen impaction, otitis media, or eustachian tube dysfunction) may also be associated with subjective tinnitus, by altering sound input to the central auditory system.
Objective tinnitus represents actual noise generated by physiologic phenomena occurring near the middle ear. Usually the noise comes from blood vessels, either normal vessels in conditions of increased or turbulent flow (eg, caused by atherosclerosis) or abnormal vessels (eg, in tumors or vascular malformations). Sometimes muscle spasms or myoclonus of palatal muscles or muscles in the middle ear (stapedius, tensor tympani) cause clicking sounds.
Causes may be considered by whether they cause subjective or objective tinnitus (see Some Causes of Tinnitus).
Subjective tinnitus may occur with almost any disorder affecting the auditory pathways.
The most common disorders are those that involve sensorineural hearing loss, particularly
Infections and CNS lesions (eg, caused by tumor, stroke, multiple sclerosis) that affect auditory pathways also may be responsible.
Disorders causing conductive hearing loss also may cause tinnitus. These include obstruction of the ear canal by cerumen, a foreign body, or external otitis. Otitis media, barotrauma, eustachian tube dysfunction, and otosclerosis may also be associated with tinnitus.
Temporomandibular joint dysfunction may be associated with tinnitus in some patients.
Objective tinnitus usually involves noise from vascular flow, which causes an audible pulsating sound synchronous with the pulse. Causes include
Muscle spasms or myoclonus of palatal muscles or those of the middle ear (stapedius, tensor tympani) may cause perceptible noise, typically a rhythmic clicking. Such spasms may be idiopathic or caused by tumors, head trauma, and infectious or demyelinating diseases (eg, multiple sclerosis). Palatal myoclonus causes visible movement of the palate, tympanic membrane, or both that coincides with tinnitus.
Some Causes of Tinnitus
History of present illness should note duration of tinnitus, whether it is in one or both ears, and whether it is a constant tone or intermittent. If intermittent, the clinician should determine whether it is regular and whether it is about the rate of the pulse or sporadic. Any exacerbating or relieving factors (eg, swallowing, head position) should be noted. Important associated symptoms include hearing loss, vertigo, ear pain, and ear discharge.
Review of systems should seek symptoms of possible causes, including diplopia and difficulty swallowing or speaking (lesions of the brain stem) and focal weakness and sensory changes (peripheral nervous system disorders). The impact of the tinnitus on the patient also should be assessed. Whether the tinnitus is sufficiently distressing to cause significant anxiety, depression, or sleeplessness should be noted.
Past medical history should ask about risk factors for tinnitus, including exposure to loud noise, sudden pressure change (from diving or air travel), history of ear or CNS infections or trauma, radiation therapy to the head, and recent major weight loss (risk of eustachian dysfunction). Drug use should be ascertained, particularly any salicylates, aminoglycosides, or loop diuretics.
Physical examination focuses on the ear and the nervous system.
The ear canal should be inspected for discharge, foreign body, and cerumen. The tympanic membrane should be inspected for signs of acute infection (eg, redness, bulging), chronic infection (eg, perforation, cholesteatoma), and tumor (red or bluish mass). A bedside hearing test should be done.
Cranial nerves, particularly vestibular function (see page Dizziness and Vertigo), are tested along with peripheral strength, sensation, and reflexes. A stethoscope is used to listen for vascular noise over the course of the carotid arteries and jugular veins and over and adjacent to the ear.
In some cases, tinnitus may indicate retrocochlear pathology, such as an acoustic neuroma (benign but invasive tumor originating from the vestibular portion of the 8th cranial nerve in the internal auditory canal).
It is important to note whether the tinnitus is unilateral because acoustic neuromas may manifest only with unilateral tinnitus. This diagnosis is more likely if there is also unilateral sensorineural hearing loss or asymmetric hearing loss with worse hearing in the ear with tinnitus.
It also is important to distinguish the uncommon cases of objective tinnitus from the more common cases of subjective tinnitus. Tinnitus that is pulsatile or intermittent is almost always objective (although not always detectable by the examiner), as is that associated with a bruit. Pulsatile tinnitus is nearly always benign. Continuous tinnitus is usually subjective (except perhaps for that caused by a venous hum, which may be identified by presence of a bruit and often by a change in tinnitus with head rotation or jugular vein compression).
Specific causes can often be suspected by findings on examination (see Some Causes of Tinnitus). In particular, exposure to loud noise, barotrauma, or certain drugs before onset suggests those factors as the cause.
All patients with significant tinnitus should be referred for comprehensive audiologic evaluation to determine the presence, degree, and type of hearing loss.
In patients with unilateral tinnitus and hearing loss, acoustic neuroma should be ruled out by gadolinium-enhanced MRI. In patients with unilateral tinnitus and normal hearing and physical examination, MRI is not necessary unless tinnitus persists > 6 mo.
Other testing depends on patient presentation (see Some Causes of Tinnitus).
Patients with visible evidence of a vascular tumor in the middle ear require CT, gadolinium-enhanced MRI, and referral to a subspecialist if the diagnosis is confirmed.
Patients with pulsatile, objective tinnitus and no ear abnormalities on examination or audiology require further investigation of the vascular system (carotid, vertebral, and intracranial vessels). The usual test sequence is to begin with magnetic resonance angiography (MRA). However, because MRA is not very sensitive for dural AVMs, many clinicians then consider doing an arteriogram. However, because dural AVMs are rare, the significant risks of arteriography must be weighed against the potential benefit of diagnosis and treatment (with embolization) of this vascular anomaly.
Treatment of the underlying disorder may lessen tinnitus. Correcting hearing loss (eg, with a hearing aid) relieves tinnitus in about 50% of patients.
Because stress and other mental factors (eg, depression) can exacerbate symptoms, efforts to recognize and treat these factors may help. Many patients are reassured by learning that their tinnitus does not represent a serious medical problem. Tinnitus also can be worsened by caffeine and other stimulants, so patients should try eliminating use of these substances.
Although no specific medical or surgical therapy is available, many patients find that background sound masks the tinnitus and may help them fall asleep. Some patients benefit from a tinnitus masker, a device worn like a hearing aid that provides a low-level sound that can cover up the tinnitus. Tinnitus retraining therapy, offered by programs that specialize in tinnitus treatment, are helpful for many patients. Electrical stimulation of the inner ear, as with a cochlear implant, occasionally reduces the tinnitus but is appropriate only for patients who are profoundly deaf.
Subjective tinnitus is caused by an abnormality somewhere in the auditory pathway.
Objective tinnitus is caused by an actual noise produced in a vascular structure near the ear.
Loud noise, aging, Meniere disease, and drugs are the most common causes of subjective tinnitus.
Unilateral tinnitus with hearing loss or dizziness/dysequilibrium warrants gadolinium-enhanced MRI to rule out acoustic neuroma.
Any tinnitus accompanied by a neurologic deficit is of concern.
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