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Classification and external resources
ICD-10 H93.1
ICD-9 388.3
DiseasesDB 27662
MedlinePlus 003043
eMedicine ent/235 
MeSH D014012

Tinnitus (pronounced /tɪˈnaɪtəs/ or /ˈtɪnɪtəs/,[1] from the Latin word for "ringing"[2]) is the perception of sound within the human ear in the absence of corresponding external sound.

Tinnitus can be perceived in one or both ears or in the head. It is usually described as a ringing noise, but in some patients it takes the form of a high pitched whining, buzzing, hissing, screaming, humming, or whistling sound, or as ticking, clicking, roaring, "crickets" or "tree frogs" or "locusts", tunes, songs, or beeping.[3] It has also been described as a "wooshing" sound, as of wind or waves.[4]. Tinnitus can be intermittent or it can be continuous. In the latter case, this "phantom" sound can create great distress in the sufferer.

Tinnitus is not itself a disease but a symptom resulting from a range of underlying causes. Causes include ear infections, foreign objects or wax in the ear, nose allergies that prevent (or induce) fluid drain and cause wax build-up, and injury from loud noises. Tinnitus is also a side-effect of some oral medications, such as aspirin, and may also result from an abnormally low level of serotonin activity. It is also a classical side effect of Quinidine, a Class IA anti-arrhythmic. In many cases, however, no underlying physical cause can be identified.

The sound perceived may range from a quiet background noise to one that can be heard even over loud external sounds. The term "tinnitus" usually refers to more severe cases. Heller and Bergman (1953) conducted a study of 80 tinnitus-free university students placed in an anechoic chamber and found that 93% reported hearing a buzzing, pulsing or whistling sound. Cohort studies have demonstrated that damage to hearing (among other health effects) from unnatural levels of noise exposure is very widespread in industrialized countries.[5]

Because tinnitus is often defined as a subjective phenomenon, it is difficult to measure using objective tests, such as by comparison with noise of known frequency and intensity, as in an audiometric test. The condition is often rated clinically on a simple scale from "slight" to "catastrophic" according to the practical difficulties it imposes, such as interference with sleep, quiet activities, and normal daily activities.[6] For research purposes, the more elaborate Tinnitus Handicap Inventory is often used.[6][7]


[edit] Objective tinnitus

In some cases, a clinician can perceive an actual sound (e.g., a bruit) emanating from the patient's ears. This is called objective tinnitus. Objective tinnitus can arise from muscle spasms that cause clicks or crackling around the middle ear.[8] Some people experience a sound that beats in time with the pulse (pulsatile tinnitus).[9] Pulsatile tinnitus is usually objective in nature, resulting from altered blood flow or increased blood turbulence near the ear (such as from atherosclerosis or venous hum[10]), but it can also arise as a subjective phenomenon from an increased awareness of blood flow in the ear.[9] Rarely, pulsatile tinnitus may be a symptom of potentially life-threatening conditions such as carotid artery aneurysm[11] or carotid artery dissection.[12]

[edit] Measuring tinnitus

The basis of quantitative measurement of tinnitus relies on the brain’s tendency to select out only the loudest sounds heard. Based on this tendency, the amplitude of a patient's tinnitus can be measured by playing sample sounds of known amplitude and asking the patient which he or she hears. The tinnitus will always be equal to or less than sample noises heard by the patient. This method works very well to gauge objective tinnitus (see above.) For example: if a patient has a pulsatile paraganglioma in his ear, he will not be able to hear the blood flow through the tumor when the sample noise is 5 decibels louder than the noise produced by the blood. As sound amplitude is gradually decreased, the tinnitus will become audible, and the level at which it does so provides an estimate of the amplitude of the objective tinnitus.

Objective tinnitus, however, is quite uncommon. Often patients with pulsatile tumors will report other coexistent sounds, distinct from the pulsatile noise, that will persist even after their tumor has been removed. This is generally subjective tinnitus, which, unlike the objective form, cannot be tested by comparative methods.

If a subject is focused on a sample noise, they can often detect it to levels below 5 decibels, which would indicate that their tinnitus would be almost impossible to hear. Conversely, if the same test subject is told to focus only on their tinnitus, they will report hearing the sound even when test noises exceed 70 decibels, making the tinnitus louder than a ringing phone. This quantification method suggests that subjective tinnitus relates only to what the patient is attempting to hear. Patients actively complaining about tinnitus could thus be assumed to be people who have become obsessed with the noise. This is only partially true. The problem is involuntary; generally complaining patients simply cannot override or ignore their tinnitus. The noise is often present in both quiet and noisy environments, and can become quite intrusive to their daily lives.

Subjective tinnitus may not always be correlated with ear malfunction or hearing loss. Even people with near-perfect hearing may still complain of it. Tinnitus may also have a connection to memory problems, anxiety, fatigue or a general state of poor health.

[edit] Mechanisms of subjective tinnitus

One of the possible mechanisms relies in the otoacoustic emissions. The inner ear contains thousands of minute hairs, called stereocilia, which vibrate in response to sound waves and cells which convert neural signals back into acoustical vibrations. The sensing cells are connected with the vibratory cells through a neural feedback loop, whose gain is regulated by the brain. This loop is normally adjusted just below onset of self-oscillation, which gives the ear spectacular sensitivity and selectivity. If something changes, it's easy for the delicate adjustment to cross the barrier of oscillation and tinnitus results. This can actually be measured by a very cells. Listening to loud music kills our hair cells, and studies have that as we lose hair cells, afferent neurons are activated, activating auditory parts of the brain and giving the perception of sound.[citation needed]

Other possible mechanisms of how things can change in the ear is damage to the receptor cells. Although receptor cells can be regenerated from the adjacent supporting Deiters cells after injury in birds, reptiles, and amphibians, in mammals it is believed that they can be produced only during embryogenesis. Although mammalian Deiters cells reproduce and position themselves appropriately for regeneration, they have not been observed to transdifferentiate into receptor cells except in tissue culture experiments.[13][14] Therefore, if these hairs become damaged, through prolonged exposure to excessive decibel levels, for instance, then deafness to certain frequencies occurs. In tinnitus, they may falsely relay information at a certain frequency that an externally audible sound is present, when it is not.

The mechanisms of subjective tinnitus are often obscure. While it is not surprising that direct trauma to the inner ear can cause tinnitus, other apparent causes (e.g., temporomandibular joint disorder (TMJ) and dental disorders) are difficult to explain. Research has proposed that there are two distinct categories of subjective tinnitus: otic tinnitus, caused by disorders of the inner ear or the acoustic nerve, and somatic tinnitus, caused by disorders outside the ear and nerve but still within the head or neck. It is further hypothesized that somatic tinnitus may be due to "central crosstalk" within the brain, as certain head and neck nerves enter the brain near regions known to be involved in hearing.[citation needed]

Studies by researchers at the University of Western Australia suggest that tinnitus is caused by increased neural activity in the auditory brainstem where the brain processes sounds, causing some auditory nerve cells to become overexcited. This in turn is related to changes in the genes involved in regulating the activity of those nerve cells. This proposed mechanism suggests possible treatments for the condition, involving the normalization or suppression of overactive neural activity through electrical or chemical means.[15]

While most discussions of tinnitus tend to stress physical mechanisms, there is strong evidence that the level of an individual's awareness of their tinnitus can be stress-related, and so should be addressed by improving the state of the nervous system generally, using gradual, unobtrusive, long-term treatments.[citation needed] [7]

[edit] Prevention

Tinnitus and hearing loss can be permanent conditions, thus, precautionary measures are advisable. If a ringing in the ears is audible after exposure to a loud environment, such as a rock concert or a work place, it means that damage may have already been done [8]. Prolonged exposure to noise levels as low as 70 dB can result in damage to hearing (see noise health effects). For musicians and DJs, special musicians' earplugs play a huge role in preventing tinnitus and can lower the volume of the music without distorting the sound and can prevent tinnitus from developing in later years. For anyone operating loud electrical appliances, such as vacuum cleaners, hair dryers, and lawn mowers, earplugs are also helpful in reducing noise exposure.

It is also important to check medications for potential ototoxicity. Ototoxicity can be cumulative between medications, or can greatly increase the damage done by noise. If ototoxic medications must be administered, close attention by the physician to prescription details, such as dose and dosage interval, can reduce the damage done.[16]

[edit] Causes of subjective tinnitus

Tinnitus can have many different causes, but most commonly results from otologic disorders – the same conditions that cause hearing loss. The most common cause is noise-induced hearing loss, resulting from exposure to excessive or loud noises. But tinnitus, along with sudden onset hearing loss, may have no obvious external cause. Ototoxic drugs can cause tinnitus either secondary to hearing loss or without hearing loss, and may increase the damage done by exposure to loud noise, even at doses that are not in themselves ototoxic.[17]

Causes of tinnitus include:[18]

[edit] Treatment

There are many treatments for tinnitus that have been claimed, with varying degrees of statistical reliability:

Objective tinnitus:

  • Gamma knife radiosurgery (glomus jugulare)[22]
  • Shielding of cochlea by teflon implant[23]
  • Botulinum toxin (palatal tremor)[24]
  • Propranolol and clonazepam (arterial anatomic variation)[25]
  • Clearing ear canal (in the case of earwax plug)[26]

Subjective tinnitus:

  • Drugs and nutrients
    • Ginkgo Biloba
    • Lidocaine, injection into the inner ear found to suppress the tinnitus for 20 minutes, according to a Swedish study.[27]
    • Benzodiazepines (lorazepam, clonazepam) in small doses
    • Tricyclics (amitriptyline, nortriptyline} in small doses [28]
    • Avoidance of caffeine, nicotine, salt[29][30][31]
    • The consumption of alcohol has been found to both increase and decrease the severity of tinnitus. Therefore, alcohol's effect on the severity of tinnitus is dependent on the causes of the individual's affliction and cannot be considered a treatment.[32][31]
    • Zinc supplementation (where serum zinc deficiency is present)[33][34][35]
    • Acamprosate[36]
    • Etidronate or sodium fluoride (otosclerosis)[37]
    • Lignocaine or anticonvulsants (usually in patients responsive to white noise masking)[38]
    • Carbamazepine[39]
    • Melatonin (especially for those with sleep disturbance)[40]
    • Sertraline[41]
    • Vitamin combinations (Lipoflavonoid)[42]
  • Electrical stimulation
    • Transcranial magnetic stimulation or transcranial direct current stimulation[43][44]
    • Transcutaneous electrical nerve stimulation[45]
    • Direct stimulation of auditory cortex by implanted electrodes[46]
    • Berthold Langguth, German neurologist would apply an electric or magnetic current for stimulation over the head of the patient to reduce ringing sound. Dirk De Ridder, Belgian neurosurgeon implanted electrodes to the brain of sufferers to normalise overactive neurons. Cambridge scientists also found that lidocaine, an anaesthetic reduces the sound in 2/3 of patients for 5 minutes, but it needs another drug to suppress its dangerous effects.[47]
  • Surgery
    • Repair of perilymph fistula[48]
  • External sound
  • Psychological
  • Light-based

[edit] Notable individuals with tinnitus

Notable sufferers of tinnitus include:

[edit] See also

[edit] Books

  • Laurence McKenna; Gerhard Andersson; Baguley, David (2005). Tinnitus: A Multidisciplinary Approach. Whurr Publishers, Ltd. ISBN 1-86156-403-1. 
  • "Tinnitologia" Ramiro M. Vergara. (ISBN 9789584419309), Lulu.com, 2008

[edit] References

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  4. ^ MedlinePlus Encyclopedia Ear noises or buzzing
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[edit] External links

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