Tinnitus is not a disease; but a symptom resulting from a range of underlying causes that can include: ear infections, foreign objects or wax in the ear, nose allergies that prevent (or induce) fluid drain and cause wax build-up. Tinnitus can also be caused by natural hearing impairment (as in aging), as a side-effect of some medications, and as a side-effect of genetic (congenital) hearing loss. However, the most common cause for tinnitus is noise-induced hearing loss.
As tinnitus is usually 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.
Tinnitus is common. About one in five people between 55 and 65 years old report tinnitus symptoms on a general health questionnaire and 11.8% on more detailed tinnitus-specific questionnaires.
Characteristics
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, tinging or whistling sound, or as ticking, clicking, roaring, "crickets" or "tree frogs" or "locusts," tunes, songs, beeping, or even a pure steady tone like heard in a hearing test.It has also been described as a "wooshing" sound, as of wind or waves. Tinnitus can be intermittent or it can be continuous in which case it can be the cause of great distress. In some individuals, the intensity of tinnitus can be changed by shoulder, head, tongue, jaw, or eye movements.
Most people with tinnitus have hearing loss,in that they are often unable to properly hear external sounds which occur within the same range of frequencies as their "phantom sounds." This has led to the suggestion that one cause of tinnitus might be a homeostatic response of central dorsal cochlear nucleus auditory neurons that makes them hyperactive in compensation to auditory input loss.
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 100 tinnitus-free university students placed in ananechoic 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.
For research purposes, the more elaborate Tinnitus Handicap Inventory is often used. Persistent tinnitus may cause irritability, fatigue, and on occasions clinical depression and musical hallucinations.
As with all diagnostics, other potential sources of the sounds normally associated with tinnitus should be ruled out. for instance, two recognized sources of very high pitched sounds might be electromagnetic fields common in modern wiring, and various sound signal transmissions.
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.Some people experience a sound that beats in time with the pulse (pulsatile tinnitus or vascular tinnitus).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), but it can also arise as a subjective phenomenon from an increased awareness of blood flow in the ear.Rarely, pulsatile tinnitus may be a symptom of potentially life-threatening conditions such as carotid artery aneurysm or carotid artery dissection. Pulsatile tinnitus may also indicate vasculitis, or more specifically, giant cell arteritis.
Measuring tinnitus
The basis of quantitatively measuring 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, he can often detect it to levels below 5 decibels, which would indicate that his tinnitus would be almost impossible to hear. Conversely, if the same test subject is told to focus only on the tinnitus, he 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. Whilst it is tempting to assume that patients actively complaining about tinnitus have simply become obsessed with the noise, this is only partially true. The noise is often present in both quiet and noisy environments, and can become quite intrusive to their daily lives. The problem is involuntary; generally, complaining patients simply cannot override or ignore their tinnitus.
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.
Mechanisms of subjective tinnitus
One of the possible mechanisms relies on 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. Listening to loud music kills hair cells, and studies have shown that as hair cells are lost, different neurons are activated, activating auditory parts of the brain and giving the perception of sound.
Another possible mechanism underlying tinnitus 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 duringembryogenesis. 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.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 (TMJD or TMD) 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, andsomatic 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.
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. The basis of this theory is that most people with tinnitus also have hearing loss and the frequencies they cannot hear link to the subjective frequencies of their tinnitus.Models of hearing loss and the brain support the idea that a homeostatic response of central dorsal cochlear nucleus neurons could result in them being hyperactive in a compensation process to the loss of hearing input.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.
While most discussions of tinnitus tend to emphasize physical mechanisms, there is strong evidence that the level of an individual's awareness of his or her 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.
Prevention
Tinnitus and hearing loss can be permanent conditions, and therefore precautionary measures are advisable. If a ringing in the ears is audible following lengthy exposure to a source of loud noise, such as a music concert or an industrial workplace, it means that lasting damage may already have occurred.
Prolonged exposure to sound/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 using loud electrical appliances, such as hair dryers, vacuum cleaners or noisy environments such as building sites where earmuffs are impractical, earplugs are also helpful in reducing noise exposure. For operating lawn mowers, hammer drills, grinders, and similar, earmuffs may be more appropriate for hearing protection.
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.
Causes of subjective tinnitus
Subjective tinnitus can have many possible 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 subjective 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.
Subjective tinnitus is also a side-effect of some oral medications, such as aspirin, and may also result from an abnormally low level of serotoninactivity. It is also a classical side effect of quinidine, a Class IA anti-arrhythmic. Over 260 medications have been reported to cause tinnitus as a side effect. In many cases, however, no underlying physical cause can be identified.
Causes of subjective tinnitus include:
Otologic problems and hearing loss:
conductive hearing loss
external ear infection
acoustic shock
drums[citation needed]
subwoofers[31]
cerumen (earwax) impaction
middle ear effusion
Superior canal dehiscence
sensorineural hearing loss
excessive or loud noise
presbycusis (age-associated hearing loss)
Ménière's disease
acoustic neuroma
mercury poisoning or lead poisoning
ototoxic medications
analgesics:
aspirin
nonsteroidal anti-inflammatory drugs
antibiotics:
aminoglycosides e.g. gentamicin
chloramphenicol
erythromycin
tetracycline
tobramycin
vancomycin
Vibramycin (doxycycline)
chemotherapy and antiviral drugs:
bleomycin
interferon
pegylated interferon-alpha-2b
cisplatin
mechlorethamine
methotrexate
vincristine
loop diuretics:
bumetanide
ethacrynic acid
furosemide
others:
chloroquine
quinine
anti-depressants
Champix
Psychedelic drugs:
5-MeO-DET
5-Methoxy-diisopropyltryptamine
Diisopropyltryptamine (DiPT)
Harmaline
,N-dimethyltryptamine
Psilocybin
Salvinorin A
neurologic disorders:
chiari malformation
multiple sclerosis
head injury
skull fracture
closed head injury
whiplash injury
temporomandibular joint disorder
giant cell arteritis
metabolic disorders:
thyroid disorder
hyperlipidemia
vitamin B12 deficiency
Iron deficiency anemia
psychiatric disorders:
depression
anxiety
other causes:
Tension myositis syndrome
fibromyalgia
vasculitis
hypertonia (muscle tension)
thoracic outlet syndrome
lyme disease
hypnagogia
sleep paralysis
glomus tympanicum tumor
anthrax vaccines which contain the Anthrax Protective Antigen