Dr. T. Balasubramanian M.S. D.L.O.
Definition: Tinnitus could be defined as perception of noise in the absence of acoustic stimuli. It is actually an aberrent phenomenon unrelated to the external source of sound. This sound actually creates an impression as if it is arising from within the head.
History: Attempts to classify and treat tinnitus dates back to ancient Egypt. Egyptians termed this condition as the bewitched ear. Infusions have been described that could treat tinnitus. Egyptians classified tinnitus into three types: 1. singing, 2. whispering and 3. speaking.
Prevalance: Studies have shown that nearly 20% of adults experience tinnitus in one form or the other. Factors affecting the prevalance of tinnitus include: age, gender, race, economic status, hearing loss and noise exposure.
Age: The incidence of tinnitus exponentially increases with age. This increased incidence does not seem to be influenced by noise exposure.
Sex: Men seem to be at higher risk for the development of tinnitus than women.
Race: Caucasians are at a higher risk than Africans.
Economic status: Tinnitus is common in persons belonging to lower socio economic groups
Hearing loss: Studies conducted in Canada showed people with deafness had increased incidence of tinnitus. This was regardless of the frequency affected by the hearing loss.
Noise exposure: increased the incidence of tinnitus.
Tinnitus in children: Increased incidence of otitis media in pediatric age group plays an important role in high prevalance of tinnitus in children.
Classification of tinnitus: One simplistic classification of tinnitus could be Subjective and Objective tinnitus.
Subjective tinnitus: Also known as "tinnitus aurium"is heard only by the patient. It can even be termed as auditory hallucination.
Auditory hallucinations: Are perception of meaningful sounds such as music or speech. The last two types are nothing by phanthom sensations.
Objective tinnitus: is heard both by the patient and examiner. It has an identifiable acoustic source. This type of tinnitus can further be subclassified into Pulsatile and Non pulsatile types. This classification is dependent on the patient's description of the tinnitus.
Pulsatile tinnitus: May be classified into vascular and non vascular types according to its etiology. Vascular types may further be subclassified into arterial and venous causes. Arterial causes include atherosclerosis, AV fistulas / malformations, hypertension etc. Venous causes include benign intracranial hypertension, high jugular bulb and hydrocephalus.
Non vascular types of pulsatile tinnitus include palatal myoclonus, tensor tympani myoclonus, and stapedial myoclonus.
Non pulsatile tinnitus should be differentiated into mild and severe types.
Classification schemes available: Various classification schemes have been suggested by various authors.
1. Goodhill scheme
2. Nodar scheme
3. Shulman scheme
Goodhill classification: This system has three sections: 1. Head noises versus aural noises, 2. Vibratory versus nonvibratory tinnitus, and 3. composition and ability to cope with tinnitus. The main advantage of this scheme is that the physician need to choose from only two options under each descriptive category. This system however has not gained wide acceptance.
Nodar's classification: This classification was based on the importance of 6 factors related to tinnitus. These include:
1. Description, 2. presence, 3. continuous or pulsatile, 4. single or multiple, 5. level and 6. annoyance. These variables are more or less similar to that of Nodar's classification, but a little simpler and user friendly. This system of classification has also not found wide use.
Shulman's classification: This classification divides tinnitus into two main categories: otologic and neurotologic. Patients belonging to otologic category include those with disease of external or middle ear, cerumen impaction, abnormal mobility of ear drum or ossicular chain, and abnormal contractions of the middle ear musculature.
The neurotologic classification is based on a complete cochlear - vestibular evaluation. It includes history and physical examination, audiological testing, vestibular evaluation and radiologic studies. Cochlear evaluation include: pure tone audiometry, auditory brain stem response, speech audiometry, tone decay testing and tests for recruitment. Vestibular testing include complete electronystagmography.
Modified Nodar's classification: In 1996 Nodar came out with a new version of his classification. He used the pneumonic ABC and C-CLAP. The term ABC denotes aurium (one ear), binaural (two ears), and cerebri (centered in the head). C-CLAP denotes cause, composition (patient's description), loudness, annoyance and pitch. This is the commonly used classification system in use these days.
Pathophysiology of tinnitus:
Subjective tinnitus is the most common type of tinnitus seen affecting the patients. This type of tinnitus is perception of sound in the absence of any physical sound. It is only possible to evaluate the nature and strength of subjective tinnitus. In majority of cases subjective tinnitus is associated with hearing loss. Tinnitus can also occur in patients with normal hearing.
Subjective tinnitus can be compared to phantom sensations which occur after amputation of limb.
The most accepted theory of tinnitus pathophysiology is that of outer hair cell damage. Alteration in the stereocilia that are attached to the outer hair cells could be the exact cause. The stiffness of the stereocilia is altered causing its decoupling from the tectorial membrane. In normal individuals these outer hair cells keep discharging spontaneously. This spontaneous discharge acts as a carrier for sound information and increases the sensitivity of brain to the sound. Since spontaneous discharge from these hair cells are normal, brain learns to adapt to this signal by largely ignoring it. When this spontaneous discharge rate rises above the background level tinnitus becomes really troublesome.
Auditory feed back system and its role in tinnitus generation: The optimal operation of auditory system is dependent on very sensitive and complex feed back mechanisms involving the afferent (ascending), efferent (descending) pathways. The auditory pathway is also linked with other extra auditory structures like reticular (serotonergic), somatosensory, hypothalamic and limbic systems thus making a tight integration with the central nervous system network. The afferent pathways described above is purely excitatory in nature, where as the efferent pathways are inhibitory in nature.The continuing interaction between these two channels creates a highly dynamic system in which pathological change at one level may have functional consequences at other levels of auditory system. For example, a noise induced cochlear lesion followed by a decrease in auditory input leads to compensatory disinhibition in the proximay auditory pathways leading on to a tonotopic reorganisation. This could form the basis for the generation of tinnitus.
Sites from where subjective tinnitus is generated:
1. Tinnitus could be generated from the inner ear due to abnormal activity of hair cells of the cochlea.
2. Abnormal function of auditory nerve can cause tinnitus
3. Brain can be one of the places from which tinnitus could be generated.
Diagram showing the areas from where tinnitus could be generated.
Tinnitus generated from the ear: Commonly Meniere's disease cause roaring tinnitus. This disorder includes a triad of symptoms which include fluctuating hearing loss, roaring tinnitus and vertigo. Some forms of tinnitus gets alleviated by sectioning of auditory nerve, thus attributing auditory nerves as a possible site of generation. Electrical current when passed through cochlea can reduce tinnitus in some patients. This beneficial effect occurs in patients in whom there is deprivation of nerual activity in the auditory nerve. Cochlear implants can alleviate tinnitus in some patients, this goes to proove the hypothesis as correct. Even the presence of wax in the external canal can cause tinnitus by blocking out the ambient noise and making the patient aware of the body sounds.
Exposure to loud sounds / exposure to ototoxic drugs can cause tinnitus associated with hearing loss. Noise and ototoxic drugs cause damage to hair cells of cochlea depriving auditory input to the brain. Brain responds to this lack of input by generating tinnitus. This is known as neural plasticity. Neural plasticity shifts the function of injured structures to other parts of the CNS. This is otherwise known as good plasticity. There is also one more type of plasticity known as the bad plasticity. Bad plasticity causes hypersensitivity and hyperacitivity by redirecting information to other parts of central nervous system by unmasking dormant synapses. It has also been suggested that phase locking of the activity in many nerve fibers can also be a cause for tinnitus.
Nervous system as the site of tinnitus: Most forms of severe tinnitus have been shown to be caused by abnormal functioning of the nervous system. Neural plasticity plays an important role here. Commonly tinnitus is accompanied by hyperacusis and phonophobia. These features are caused by changes in the function of nuclei in the ascending pathways, or by redirection of information to regions of CNS that normally donot receive inputs from the auditory system.
Tinnitus always accompanies vestibular schwannomas. Infact tinnitus could be the first symptom of a vestibular schwannoma, it becomes worse after surgical removal of schwannoma. This indicates that tinnitus could be generated by the brain in response to lack of normal stimuli from the auditory system.
Vascular contact with the intracranial portion of auditory nerve is regularly associated with tinnitus. Tinnitus in these patients disappear when the offending vessel is removed from the nerve. This type of tinnitus occur due to irritation to the nerve by the offending vessel (kindling phenomenon).
Auditory hallucinations: are generated by central nervous system. Temporal lobe tumors must be ruled out in all these patients. This type of hallucinations occur in patients with psychiatric disorders like schizophrenia. It can also occur when ketamine like drugs are used as an anesthetic.
Importance of medical history in patients with tinnitus:
A good history is a must for accurate diagnosis of the underlying pathology leading on to tinnitus.
1. Onset and duration of tinnitus
2. Subjective tinnitus should be differentiated from objective tinnitus. Subjective tinnitus is usually high pitched and ringing in nature and can only be perceived by the patient. Whereas objective tinnitus is commonly pulsatile in nature and is also heard by the examiner.
Etiology of objective tinnitus include: intracranial vascular anamolies, atherosclerosis of aorta, pseudotumor cerebri, chemodectomas involving the middle ear.
3. Unilateral and bilateral tinnitus should be differentiated
4. Severity of tinnitus should be assessed (ie whether present throughout the day - severe tinnitus, present only in the absence of ambient noise - night times - mild tinnitus).
5. The patient is asked to describe the frequency of tinnitus. In Meniere's disease it is low frequency, while in noise indued tinnitus it is of high frequency.
6. Patient is asked to grade the tinnitus using a 1 - 10 scale. Questionnaires have been designed to help the patient in this direction. The questionnaires include:
a. Tinnitus effects questionnaire
b. Tinnitus handicap questionnaire
c. Tinnitus severity scale
d. Tinnitus handicap inventory
The current questionnaire used is called CHIMPS.
This contains 6 questions namely:
1. Concentration - does the tinnitus interfere with the patient's ability to concentrate
2. Hearing - does the tinnitus interfere with the patient's ability to hear television
4. Masking - does the surrounding ambient noise covers up the tinnitus?
5. Psychologic - does the tinnitus makes the patient feel depressed or anxious?
Diagram showing the causes of tinnitus
Investigating a tinnitus patient:
After a detailed history, audiological assessment is a must. These tests include:
2. Pure tone audiometry - to assess the sensitivity of hearing
3. Tympanometry and stapedial reflex test - to identify middle ear pathology and evaluate the neural pathway for stapedial reflex.
4. OAE - to obtain additional information on cochlear and efferent function
5. Auditory brain stem evoked responses - to exclude retrocochlear pathology
Imaging: include contrast MRI / HRCT. These imaging modalities help to rule out vestibular schwannoma.
Measuring tinnitus serves to authenticate the presence of tinnitus. It also helps in deciding the optimal treatment modality. Measurments of tinnitus include assessment of the pitch, bandwidth, loudness, maskability of tinnitus and residual inhibition.
Pitch estimation: Pitch estimation of tinnitus helps in the probable etiology for tinnitus. High pitched tinnitus is common in patients with noise induced hearing loss, and low pitched tinnitus is commonly seen in Menier's disease. The patient is asked to match the tinnitus frequency with that of pure tone frequency. This test is a gross estimation of frequency of tinnitus.
Loudness: Tinnitus loudness is defined as magnitude of intensity of tinnitus. This is an index of number of nerve fibers involved. In tinnitus loudness match the patient is instructed to match the loudness of tinnitus with that of narrow band noise generated at about the same frequency as the tinnitus.
Masking: Refers to the reduction of audibility of tinnitus when the patient is exposed to another sound. This is known as tinnitus masking. The instrument used is known as the tinnitus masker. The masking noise can either be applied to the ipsilateral or contralateral ear. A single pure tone masking tone of any frequency may mask a broad band spectrum of tinnitus.
Residual inhibition: This is defined as suppression / complete elimination of tinnitus for varying periods of time following masking. This masking procedure is also known as central masking.
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