Traumatic Brain Injury : An acute injury on the brain that can range from mild to severe.
Tourette’s Syndrome : A severe neurological disorder characterized by multiple facial and other body involuntary movements, usually beginning in childhood or adolescence and often accompanied by compulsive utterances, for example, interjections and obscenities. Also called Gilles de la Tourette syndrome
Tinnitus: The perception of the presence of a sound in one or both ears that is not associated with an external sound source. Tinnitus can be described as constant or intermittent and of various volume levels, pitches, and complexities (ringing, roaring, hissing, crickets, whistling, rushing, etc).
Sensation of a ringing, roaring, or buzzing sound in the ears or head. It is often associated with many forms of hearing loss and noise exposure. Tinnitus from the Latin word tinnītus meaning “ringing”) is the perception of sound within the human ear in the absence of corresponding external sound. Tinnitus is not a disease, but a condition that can result from a wide range of underlying causes: neurological damage (multiple sclerosis), ear infections, foreign objects in the ear, nasal allergies that prevent (or induce) fluid drain, or wax build-up. Withdrawal from a benzodiazepine addiction may cause tinnitus as well. In-ear headphones, whose sound enters directly into the ear canal without any opportunity to be deflected or absorbed elsewhere, are a common cause of tinnitus when volume is set beyond moderate levels.
Tinnitus may be an accompaniment of sensorineural hearing loss or congenital hearing loss, or it may be observed as a side effect of certain medications. However, the most common cause 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 20% of people between 55 and 65 years old report symptoms on a general health questionnaire, and 11.8% on more detailed tinnitus-specific questionnaires.
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, electric buzzing, hissing, humming, tinging or whistling sound, or as ticking, clicking, roaring, “crickets” or “tree frogs” or “locusts (cicadas)”, tunes, songs, beeping, sizzling, sounds that slightly resemble human voices or even a pure steady tone like that heard during a hearing test. It has also been described as a “whooshing” 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 can be changed by shoulder, head, tongue, jaw, or eye movements.
Most people with tinnitus have some degree of hearing loss, in that they are often unable to hear clearly external sounds that 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 an anechoic chamber and found 93% reported hearing a buzzing, pulsing or whistling sound. Cohort studies have demonstrated 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 (THI) 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. A common and often misdiagnosed condition that mimics tinnitus is Radio Frequency (RF) hearing, in which subjects have been tested and found to hear high-pitched transmission frequencies that sound similar to 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. Pulsatile tinnitus may also be an indication of idiopathic intracranial hypertension.
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. 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 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. Over 260 medications have been reported to cause tinnitus as a side effect. In many cases, however, no underlying physical cause can be identified.
Tinnitus can also occur due to the discontinuation of therapeutic doses of benzodiazepines as part of the benzodiazepine withdrawal syndrome. It can sometimes be a protracted symptom from benzodiazepine withdrawal and persist for many months.
Causes of subjective tinnitus include:
- Otologic problems and hearing loss:
- conductive hearing loss
- external ear infection
- acoustic shock
- loud noise or music
- 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 or lead poisoning
- ototoxic medications
- nonsteroidal anti-inflammatory drugs
- aminoglycosides, e.g., gentamicin
- doxycycline (Vibramycin)
- chemotherapy and antiviral drugs:
- pegylated interferon-alpha-2b
- loop diuretics:
- ethacrynic acid
- varenicline (Champix)
- conductive hearing loss
- Neurologic disorders:
- chiari malformation
- multiple sclerosis
- head injury
- skull fracture
- closed head injury
- whiplash injury
- temporomandibular joint disorder
- giant cell arteritis
- Metabolic disorders:
- thyroid disease
- vitamin B 12 deficiency
- iron deficiency anemia
- psychiatric disorders:
- other causes:
- tension myositis syndrome
- hypertonia (muscle tension)
- thoracic outlet syndrome
- Lyme disease
- sleep paralysis
- glomus tympanicum tumor
- anthrax vaccines which contain the anthrax protective antigen
- Some psychedelic drugscan produce temporary tinnitus-like symptoms as a side effect
- diisopropyltryptamine (DiPT)
- benzodiazepine withdrawal
- nasal congestion
- intracranial hyper or hypotension caused by for example, Encephalitis or a cerebrospinal fluid leak
One of the possible mechanisms relies on otoacoustic emissions. The inner ear contains thousands of minute inner hair cells with stereocilia which vibrate in response to sound waves, and outer hair cells which convert neural signals into tension on the vibrating basement membrane. 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 is easy for the delicate adjustment to cross the barrier of oscillation, and tinnitus results. Exposure to excessive sound kills hair cells, and studies have shown 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 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. Therefore, if these hairs become damaged, through prolonged exposure to excessive sound levels, for instance, then deafness to certain frequencies results. In tinnitus, they may relay information that an externally audible sound is present at a certain frequency 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 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 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 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 most people with tinnitus also have hearing loss, and the frequencies they cannot hear are similar to the subjective frequencies of their tinnitus.Models of hearing loss and the brain support the idea 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 her or his 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.
Since some tinnitus mimics electronic sounds, some recent research is focusing on electronics, the prolonged use of cell phones, and other modern electronic devices as possible causes. These findings are consistent with reviews of older research associating tinnitus with prolonged exposure to electromagnetic radiation.
Tinnitus is commonly thought of as a symptom of adulthood; this may be why tinnitus in children is generally overlooked. Children with hearing loss have a high incidence of tinnitus, even though they do not express that they have tinnitus and the effect it has on their lives (Celik et al., 2009). Children do not generally report tinnitus spontaneously and their complaints may not be taken seriously (Mills et al., 1986). Among those children who do complain of tinnitus, there is an increased likelihood of associated otological or neurological pathology such as migraine, juvenile Meniere’s disease or chronic suppurative otitis media (Graham and Baguley, 2009). Its reported prevalence varies from 12% to 36% in children with normal hearing thresholds and up to 66% in children with a hearing loss and aprroximately 3-10% of children have been reported to be troubled by tinnitus (Shetye and Kennedy, 2010).
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 she or he hears. The volume of the tinnitus will always be equal to or less than that of the 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 the attention of a subject is focused on a sample noise, she can often detect it at levels below 5 decibels, which would indicate her tinnitus would be almost impossible to hear. Conversely, if the same test subject is told to focus only on the tinnitus, she will report hearing the sound even when test noises exceed 70 decibels, making the tinnitus louder than a ringing phone. This quantification method suggests subjective tinnitus relates only to what the patient is attempting to hear. Whilst it is tempting to assume patients actively complaining about tinnitus have simply become obsessed with the noise, this is only partially true. The noises are 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.
Measuring tinnitus with auditory evoked response
Tinnitus is the description of a noise inside a person’s head in the absence of auditory stimulation. The noise can be described in many different ways, but the most common description of the tinnitus is a pure tone sound. Tinnitus affects one third of adults at some time in their lives, whereas ten to fifteen percent are disturbed enough to seek medical evaluation About two million Americans are so seriously disturbed by tinnitus that they cannot function on a day-to-day basis. (American Tinnitus Association, 2010).
Tinnitus can be classified as either subjective or objective. Objective tinnitus can be detected by other people and is usually caused by myoclonus or a vascular condition. Subjective tinnitus can only heard by the affected person and is caused by otology, neurology, infection, or drugs. A frequent cause of subjective tinnitus is noise exposure which damages hair cells in the inner ear causing tinnitus. Tinnitus can be associated with many emotions. It is best illustrated by Jastreboff’s Neurophysiological model.
The “Edge Effect” theory has been described by many researchers throughout the literature when discussing tinnitus. As hair cells are lost or damaged, afferent neurons generate auditory sensations at frequencies near the impaired region. This theory possibly explains why tinnitus can be associated with a reflection of hearing loss and why tinnitus can be persistent.
Some researchers believe that spontaneous otoacoustic emissions (SOAEs) may be associated with tinnitus. Processes in the cochlea can cause self oscillation that is perceived as tinnitus, but most studies found that the two phenomena are not related. The evaluation of SOAEs and tinnitus was based on pitch matching and researchers concluded that not enough evidence could be seen to make the conclusion. When the researchers used two specific criteria to evaluate the results, researchers found SOAEs and tinnitus to be related in 2.42% of subjects.
In 2010, Qasem compared the differences in outer hair cell function in normal hearing patients with and without tinnitus. Distortion product OAEs (DPOAEs) were measured and results showed significant differences between groups at all DPOAE frequencies tested. Researchers concluded that decreased DPOAE amplitude can be seen in tinnitus patients due to the association between tinnitus and reduced outer hair cell movement. This study illustrates that the outer hair cells are related to tinnitus.
Moller studied the effects of tinnitus in relation to compound action potentials (CAP) in 1992. Researchers recorded compound action potential components N1 and N2 and found that the latencies of the responses in the tinnitus patients were similar to patients with no tinnitus. This study concludes that tinnitus effects can not be observed in CAP. The effects of tinnitus on auditory brainstem response (ABR) measures have also been evaluated by many researchers. Auditory pathway plays a role in the emotional and physiological response to tinnitus. Research has shown abnormal ABR results (interwave latency delays) in patients with tinnitus. In 2008, Kehrle used ABR testing to evaluate the auditory nerve and brainstem function of tinnitus patients with normal hearing. Results showed delayed wave latencies and interpeak latencies between the tinnitus and non tinnitus patients. Researchers concluded that latency prolongations of wave I and lengthening of III-V IPL found in this study confirmed the findings in previous research. Maurizi in 1985 used ABRs to evaluate the auditory pathway in patients with tinnitus and concluded that patients with tinnitus had abnormal ABR recordings. Peripheral tinnitus was reduced with residual inhibition and recordings returned to normal. However, this method is not valid for all tinnitus patients due to the many different causes of tinnitus. Gerken in 2001 evaluated the influence of tinnitus on auditory evoked potentials. Results showed delayed ABR wave VII latencies in the tinnitus group and about half of the tinnitus patients had MLR amplitudes that were significantly greater than the control group mean. Researchers concluded the latency differences for wave VII only adds more diversity to research findings and should be included in future research. Large MLR waves seen in the tinnitus group may be caused by unknown smaller factors not accounted for in the study.
Tinnitus and auditory evoked cortical potentials have also been studied. It is important to evaluate the primary auditory cortex in relation to Jastrebroff’s model. “ALRs reflect stimulus properties as well as attention and the psychological state of the subjects, both of which are presumed to contribute to tinnitus” -Kadner (2002). Low and colleagues in 2008 concluded that ALRs can be used to evaluate the effectiveness of therapies used to alleviate tinnitus.
Tinnitus has also been studied in relation to event related potentials. In 1991, Shiraishi and colleagues found that the contingent negative variation (CNV) amplitude was significantly enlarged in tinnitus patients. They also found no effect on the latency and amplitude of the N100 and P300 responses. Attias in 1993, found that the amplitudes of N1, P2, and P3 were reduced, P3 latencies delayed, and N1 and N2 had delayed latencies to non-target stimuli.
In 2008, Delb conducted a study that evaluated tinnitus patients with high and low tinnitus related distress and how they differ in respect to focus levels on the tinnitus. Researchers concluded that patients with different levels of distress have differences in their ability to shift attention.
Elbert in 2004 studied the relation between tinnitus and mismatched negativity (MMN). Researchers recorded MMN potentials at stimulus levels at the edge frequency of the patient’s tinnitus and found differences in the recordings. This finding can be applied to tinnitus treatments to monitor progress and show effectiveness.
Tinnitus and long latency auditory evoked potentials (LLAEPs) have also been researched quite frequently. Alterations of LLAEPs have been seen in individuals with tinnitus and indicate problems in the auditory pathway in the cortex which can be concluded by increased latency values. In 2010, Santos Filha measured LLAEP potentials of tinnitus patients with a history of noise exposure. Researchers concluded that LLAEP shifts occur more often in individuals with tinnitus when compared to the control group.
In conclusion, tinnitus can be evaluated with most auditory evoked potentials; however results may be inconsistent. Results must be compared to age and hearing matched control subjects to be reliable. This inconsistently reported may be due to many reasons: differences in the origin of the tinnitus, ABR recording methods, and selection criteria of control groups. Since research shows conflicting evidence, more research on the relationship between tinnitus and auditory evoked potentials should be carried out before these measurements are used clinically.
Tinnitus and hearing loss can be permanent conditions. 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 lasting damage may have already occurred
Prolonged exposure to sound or 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 an important role in preventing tinnitus; they 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 or vacuum cleaners, or who work in noisy environments such as building sites, where earmuffs are impractical, earplugs are also helpful in reducing noise exposure. This is also the case for while riding motorcycles, mopeds etc. While 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 of multiple medicines can have a cumulative effect, and 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.
Many treatments for tinnitus have been claimed, with varying degrees of statistical reliability:
- Gamma knife radiosurgery (glomus jugulare)
- Shielding of cochlea by teflon implant
- Botulinum toxin (palatal tremor)
- Clearing ear canal (in the case of earwax plug
- Using a neurostimulator
- Drugs and nutrients
- Melatonin (especially for those with sleep disturbance)
- Lidocaine injection into the inner ear was found to suppress the tinnitus for 20 minutes, according to a Swedish study.
- Older benzodiazepines, e.g. diazepam, are sometimes used for tinnitus; however, there are significant risks associated with the long-term use of benzodiazepines.
- Tricyclics (amitriptyline, nortriptyline) in small doses
- Avoidance of caffeine, nicotine, or salt can reduce symptoms, but, tinnitus can also be induced by reducing caffeine and/or smoking.
- 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.
- Zinc supplementation (where serum zinc deficiency is present)
- Etidronate or sodium fluoride (otosclerosis)
- Lignocaine or anticonvulsants (usually in patients responsive to white noise masking)
- Vitamin combinations (lipoflavonoid)
- Electrical stimulation
- Transcranial magnetic stimulation or transcranial direct current stimulation
- Transcutaneous electrical nerve stimulation
- Direct stimulation of auditory cortex by implanted electrodes
- Berthold Langguth, a German neurologist, would apply an electric or magnetic current for stimulation over the head of the patient to reduce the ringing sound. Dirk De Ridder, a Belgian neurosurgeon, implanted electrodes to the brain of sufferers to normalise overactive neurons. Cambridge University scientists also found lidocaine, an anaesthetic, reduces the sound in 2/3 of patients for 5 minutes, but it needs another drug to suppress its dangerous effects.
- Vagus nerve stimulation
- Repair of the perilymph fistula
- External sound
- Low-pitched sound treatment has shown some positive, encouraging results.(UC, Irvine press release)
- Tinnitus masker (e, or better ‘shaped’ or filtered noise)
- Tinnitus retraining therapy
- Auditive stimulation therapy (music therapy)
- Auditive destimulation therapy (also called “notched music” therapy) uses individually designed music with the patients’ favorite music altered to remove the musical tones that match the aural frequencies associated with their tinnitus. The removal of these tones alleviates the tinnitus by destimulating brain activity for these specific frequencies.
- Compensation for lost frequencies by use of a hearing aid
- Ultrasonic bone-conduction external acoustic stimulation
- Avoidance of outside noise (exogenous tinnitus)
- Psychological cognitive behavioral therapy
The prognosis of tinnitus depends on the type and severity of the cause. For tinnitus due to acute acoustic trauma, approximately 35% of cases report subsiding tinnitus at three months after the trauma, with approximately 10% of these cases being the degree of complete disappearance of the tinnitus, as studied among young men having acquired tinnitus from gunshots.
Tympanoplasty – Surgical repair of the eardrum (tympanic membrane) or bones of the middle ear.
Telecoil – An induction coil in a hearing aid which picks up the electromagnetic signal from a telephone or loop amplification system.
Threshold – the level above which the subject gives a positive response and below which the subject does not give a response
Toggle – a switch on a hearing aid that allows the user to employ different memories for different listening situations. One memory might be set for a quiet office, while another may be set for a noisy restaurant.
Tympanogram – a graphical representation of the changes in acoustic immittance of the middle ear in response to changes in pressure.
Tympanometry – the measure of sound flowing through the middle ear in response to changes in pressure.
Throat Disorders – Disorders or diseases of the larynx (voice box), pharynx, or esophagus
Tongue – Large muscle on the floor of the mouth that manipulates food for chewing and swallowing. It is the main organ of taste, and assists in forming speech sounds.
Tourette Syndrome – Neurological disorder characterized by recurring movements and sounds (called tics)
TDD: Telecommunication device for the deaf. A special device that allows for the transmission of and reception of words over phone lines via a typewritten signal.
Tectorial membrane – a gelatinous tissue mass that is located above the hair cells. The cilia of the outer hair cells imbeds in tectorial membrane.
Telecoil: A coil placed inside of a hearing aid that picks up electro-magnetic energy emitted by certain telephones and assistive listening devices.
Temporomandibular joint – (TMJ), the hinge joint for the jaw.
Tensor tympani – a muscle residing in the semicanal of tensor tympani on the medial wall of the middle ear space whose tendon is attached to the malleus. Contraction of the tensor tympani muscle would move tympanic membrane inward and decrease the vibration of the TM by increasing the stiffness of the middle ear system. However, in humans this muscle does not appear to contract in response to loud sounds.
Tensor veli palatini – muscle of the nasopharynx, one of those responsible for opening the Eustachian tube.
Threshold Of Hearing: The lowest level that a particular sound’s presence can be perceived by an individual more than half of the time.
Tonotopic organization – the property of a structure to be organized such that different locations within the structure respond to different frequencies. (There is a different place within the structure for each frequency.)
Tragus – the skin covered appendage in front of the pinna. The tragus can be pushed inward to cover the entrance of the ear canal.
Transmitter: The portion of a CROS system that picks up a signal on one side of the head and sends it via a hard wire or an FM signal to the receiver on the other side of the head.
Trapezoid body – nerve fiber pathway in the lower brainstem that decussates from one hemisphere to the other. The trapezoid body contains a nucleus, called the nucleus of the trapezoid body.
Traveling wave – an undulating up and down motion of basilar membrane in response to sound that increases in amplitude relatively gradually until it reaches a maximum displacement point, and then decreases in amplitude rapidly just apical to that point of maximum vibration.
Tunnel of Corti – space beneath the arch of Corti.
Tuning fork – Hand-held device that produces tones that are essentially pure tones. Tuning forks of different sizes produce different frequency tones.
TTS (Temporary Threshold Shift): The presence of some degree of hearing loss, often induced by noise or chemical exposure, that recovers over time.
Tympanic Membrane: Another name for an eardrum. It is the membrane that separates the ear canal and the middle ear cavity. The tympanic membrane vibrates when hit with sound waves, causing the ossicular chain to vibrate.
Tympanometry: A test, also referred to as immittance testing, done during an audiological evaluation that helps to assess the integrity of the tympanic membrane (eardrum) and the middle ear cavity. During tympanometry testing, a probe is inserted into and sealed in the ear canal and then a reflected tone is measured as the pressure in the ear canal is changed. The results are often graphed onto a tympanogram, showing the compliance at various positive and negative pressure levels.
Tympanometry is an objective test of middle-ear function. It is not a hearing test, but rather a measure of energy transmission through the middle ear. The test should not be used to assess the sensitivity of hearing and the results of this test should always be viewed in conjunction with pure tone audiometry.
Tympanometry is a valuable component of the audiometric evaluation. In evaluating hearing loss, tympanometry permits a distinction between sensorinueural and conductive hearing loss, when evaluation is not apparent via Weber and Rinne testing. Furthermore, in a primary care setting, tympanometry can be helpful in making the diagnosis of otitis media by demonstrating the presence of a middle ear effusion.
A tone of 226Hz is generated by the tympanometer into the ear canal, where the sound strikes the tympanic membrane, causing vibration of the middle ear, which in turn results in the conscious perception of hearing. Some of this sound is reflected back and picked up by the instrument. Most middle ear problems result in stiffening of the middle ear, which causes more of the sound to be reflected back.
The general term used to describe how energy is transmitted through the middle ear is admittance. The instrument measures the reflected sound and expresses it as an admittance or compliance, plotting the results on a chart known as a tympanogram.
Normally, the air pressure in the ear canal is the same as ambient pressure. Also, under normal conditions, the air pressure in the middle ear is approximately the same as ambient pressure since the eustachian tube opens periodically to ventilate the middle ear and to equalize pressure. In a healthy individual, the maximum sound is transmitted through the middle ear when the ambient air pressure in the ear canal is equal to the pressure in the middle ear.
After an otoscopy (examination of the ear with an otoscope) to ensure that the path to the eardrum is clear and that there is no perforation, the test is performed by inserting the tympanometer probe in the ear canal. The instrument changes the pressure in the ear, generates a pure tone, and measures the eardrum responses to the sound at different pressures. This produces a series of data measuring how admittance varies with pressure, which is plotted as a tympanogram.
Type A tympanogram
Type B tympanogram
Type C tympanogram
Tympanograms are categorized according to the shape of the plot. A normal tympanogram (left) is labelled Type A. There is a normal pressure in the middle ear with normal mobility of the eardrum and the conduction bones. Type B and C tympanograms may reveal fluid in the middle ear, perforation of the tympanic membrane, scarring of the tympanic membrane, lack of contact between the conduction bones of the middle ear or a tumor in the middle ear.
The categorising of tympanometric data should not be used as a diagnostic indicator. It is merely a description of shape. There is no clear distinction between the three types, nor the two subtypes of type A, namely A and A. Only measures of static acoustic admittance, ear canal volume, and tympanometric width/gradient compared to gender, age, and race specific normative data can be used to somewhat accurately diagnose middle ear pathology along with the use of other audiometric data (e.g. air and bone conduction thresholds, otoscopic examination, normal word recognition at elevated presentation levels, etc.).
Tympanogram: A chart onto which the compliance results of tympanometry are graphed. Its used to assess the mobility of ear.