What is tinnitus?
One proposed classification of tinnitus distinguishes two main categories. Subjective tinnitus, the most common type, is perceived only by the patient, usually as a continuous “phantom” sensation. Objective tinnitus, the second type, can be heard through a stethoscope placed over head and neck structures and is frequently perceived as a pulsatile sound.
Continuous subjective tinnitus occurs in a multitude of ear conditions. It is most often encountered in the context of hearing loss due to aging, excessive noise exposure, or ototoxic medication (such as salycilates, aminoglycoside antibiotics, chemotherapeutics, and diuretics). The auditory sensation can be induced or worsened by ear infections or an excess of cerumen.
Other otologic causes are Ménière’s disease, otosclerosis, and acoustic neuroma. Neurologic conditions (multiple sclerosis, stroke, head injury), temporomandibular joint (TMJ) disorder, and metabolic and psychogenic factors can also lead to tinnitus.
The causes of continuous tinnitus are often difficult to pinpoint, and the pathophysiology is still poorly understood. Prominent theories include repetitive discharge from injured cochlear hair cells that generate continuous impulses in the auditory nerve, spontaneous auditory nerve activity, hyperactive brain stem auditory nuclei, and decreased suppression of peripheral nerve impulses by the auditory cortex. A neurobiological model that has gained acceptance includes two essential events: initial damage to peripheral auditory structures, which triggers the tinnitus, and subsequent (maladaptive) plastic changes in the central auditory pathway, with increased activity in brain stem and cortical areas.
Pulsatile tinnitus is caused by blood flow perturbations (through either normal or abnormal blood vessels near ear structures) and mechanical factors. Atherosclerosis, vascular tumors, arteriovenous malformations, aneurysms, and vascular loops often lead to unilateral tinnitus and can be identified using imaging techniques. Vascular inflammation and thrombosis are additional causes of pulsatile tinnitus. Conditions associated with high cardiac output, such as pregnancy, anemia, or an overactive thyroid, can result in tinnitus. Mechanical causes of pulsatile tinnitus are represented by open Eustachian tubes and middle-ear muscle spasms.
Patients with tinnitus report a disturbing noise localized in one or both ears and sometimes in the head. They describe it as ringing, whistling, hissing, swishing, roaring, buzzing, or clicking. Ear fullness or pain can be present. The severity ranges from an occasional awareness of the noise to a frustrating, even unbearable sound. Epidemiologic studies indicate that 25 percent of patients with tinnitus experience a pronounced discomfort, while the rest do not report significant distress. Sensations perceived as severe can result in attention deficit, anxiety, and depression. In general, pulsatile tinnitus, unilateral tinnitus, and tinnitus associated with additional ear symptoms should be investigated carefully because they can signal a potentially serious underlying disorder.
The assessment of a patient with tinnitus includes physical examination, blood pressure measurements, audiometric profile, complete blood chemistry, hematocrit and lipid levels, thyroid studies, and brain imaging. Most cases of tinnitus should be evaluated by an ear, nose, and throat (ENT) specialist.
Therapeutic steps vary according to the type of tinnitus diagnosed and how the symptoms affect a patient’s life. Specific treatment should be provided for any underlying illness. Inflammatory ear disease is treated with antibiotic and anti-inflammatory medication. Conditions such as tumors, vascular abnormalities, otosclerosis, and Ménière’s disease may warrant surgical intervention. If the tinnitus is caused by hearing damage, then reassurance is often sufficient. Hearing aids, noise-masking devices, and cognitive and behavioral therapy are sometimes recommended. Patients should avoid ototoxic medication, loud noise, and stress.
Many treatments are still in the experimental phase or have variable efficacy. Proposed pharmacologic therapies for severe cases include antianxiety and antidepressant agents, lidocaine, and carbamazepine. Drugs that improve brain metabolism (nootropics) and neurotransmitter-directed agents might prove beneficial. Additional approaches focus on neck exercises, sound therapy, acupuncture, and electrical brain stimulation.
Tinnitus has been considered a disease entity for centuries. It was only in the second half of the twentieth century that physicians were able to discriminate between various types of tinnitus and their underlying pathology. Tinnitus remains a perplexing disorder, both for the sufferer and for the physician. No single treatment is truly efficacious, especially in subjective tinnitus. Many variables are associated with this “phantom” sensation, and a multitude of biological mechanisms can cause it. Nevertheless, the neurobiology of tinnitus has become less mysterious. A growing body of research continues to unveil striking neural changes. Animal models are employed to elucidate brain activity patterns in tinnitus and to explore therapeutic avenues. As a result of this complexity, it is likely that successful therapeutic strategies will have to target multiple factors simultaneously.
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