(i) Individualized standardized treatment of subjective tinnitus.
Since tinnitus is often a concomitant symptom of a certain disease, it is important to first clarify the primary disease as much as possible. And carry out the treatment of the primary disease. After treatment of the primary disease, such as tinnitus caused by hypothyroidism, the tinnitus can disappear on its own in most patients after treatment with thyroid tablets. For tinnitus caused by cervical spondylosis, 70% of patients can have their tinnitus reduced or disappeared after active treatment of cervical spondylosis, so that the best therapeutic effect can be achieved. For those with unknown etiology, classification should be made according to the results of the specialist examination, the lesion site should be determined, and an individualized treatment plan should be formulated.
Subjective tinnitus is classified as follows according to whether it can be perceived by outsiders, the duration of the disease, the location of the lesion and the compensatory condition.
1. According to the duration of the disease, it can be classified as: acute tinnitus with a duration of 3 months; subacute tinnitus with a duration of 4 to 12 months; chronic tinnitus with a duration of >1 year.
2. According to the location of the lesion, it can be divided into external ear, middle ear, cochlear, neural, central and mixed tinnitus.
3.According to the presence or absence of secondary attention, sleep disorder, irritability, depression and other neuropsychiatric symptoms, tinnitus can be divided into compensatory and non-compensatory tinnitus.
(2) According to the severity of tinnitus and the presence of accompanying symptoms, the degree of tinnitus is divided into 6 levels.
Grade 0: No tinnitus.
Grade 1: Occasional tinnitus, but do not feel painful.
Grade 2: Persistent tinnitus that worsens when quiet.
Grade 3: Persistent tinnitus even in a noisy environment.
Grade 4: Persistent tinnitus with concentration and sleep disturbances.
Grade 5: Persistent severe tinnitus that prevents you from working.
Grade 6: Suicidal tendency of the patient due to severe tinnitus.
Since there is no good objective examination method for subjective tinnitus, the grading of tinnitus can be used as a rough judgment criterion for the efficacy of tinnitus. Namely
Cured: complete disappearance of tinnitus; Significant: improvement of tinnitus by more than two levels; Effective: improvement of tinnitus by one level; Ineffective: no significant change of tinnitus.
There are many causes of subjective tinnitus, and the following is an analysis of the mechanisms of tinnitus caused by the more common diseases and an introduction of their diagnostic and therapeutic methods.
I. Tinnitus of the external ear.
Common diseases: cerumen embolism in the external ear canal; foreign bodies in the external ear canal; cholesteatoma in the external ear canal, eczema in the external ear canal, etc.
Mechanism of production: Various substances in the external ear canal (such as hair strands; foreign bodies; cerumen; cholesteatoma; secretions, etc.) can irritate the eardrum and cause tinnitus symptoms.
Clinical features:Often tinnitus occurs during swallowing movements. Tinnitus is often low-pitched, buzzing or clattering.
Treatment:Clean the external ear canal.
Prognosis:Very good.
II. Middle ear tinnitus.
Common diseases:Secretory otitis media; chronic middle ear mastoiditis; middle ear cholesteatoma; adhesive otitis media, middle ear cholesterol granuloma, otosclerosis, etc.
Mechanism of generation:（1）The accumulation of fluid in the tympanic chamber can cause a change in the pressure state of the middle ear and cause tinnitus symptoms. (2) In a completely soundless environment, a person with normal hearing can also feel a certain amount of noise. In a familiar environment this autosomal noise is often masked by the noise of everyday life and does not attract attention. This autogenic noise can only be perceived to a certain extent. Autogenic noise is generated mainly by the sound of pulsating blood vessels in and around the vagus, breathing sounds, etc. This noise is significantly enhanced after strenuous somatic movements. Patients with conductive deafness often feel enhanced physiological noise because of the reduced masking effect of external environmental noise, as in the case of tinnitus in otosclerosis. Tinnitus is reduced after stapedial surgery because the masking effect of the external environment is reinforced again after the middle ear returns to normal. Transient-induced tinnitus is often associated with abnormal contraction of the stapedius muscle and is often caused by viral infection.
Clinical features:It is mostly low-pitched tinnitus, often accompanied by varying degrees of conductive deafness or mixed deafness. Routine examination of the ear often reveals lesions such as tympanic chamber effusion, tympanic membrane perforation, and cholesteatoma.
Treatment: Treatment is directed at different primary pathologies. Secretory otitis media should first be treated for diseases that may cause eustachian tube dysfunction such as chronic rhinosinusitis, adenoid hypertrophy, and nasopharyngeal carcinoma. Tympanic membrane puncture, incision or tube placement may be performed if necessary. Chronic otitis media requires surgical treatment. Transient-induced tinnitus can be treated with oral carbamazepine 0.1 Tid. After stapedial floor opening in patients with otosclerosis, tinnitus is reduced or disappears in 90% of patients.
Prognosis:Better. After middle ear surgery for chronic suppurative otitis media, 1/3 of patients had reduced tinnitus; 1/3 had unchanged tinnitus; 1/3 had worsened tinnitus.
Third, inner ear tinnitus.
Common diseases:low-frequency descending sensorineural deafness, Meniere’s disease, auditory neuropathy, noise injury, sudden deafness, ototoxic drug injury, etc.
Mechanism of generation:Cochlear tinnitus is the result of the auditory nerve receiving pathological excitation from the cochlea. The cochlea or cochlear nerve lesions can cause an increase in the firing rate of the inner hair cells and the nerve fibers to which they belong. Lesions of the inner ear include damage to the top of the cell and mechanical electrical transmission disorders (acute noise injury); damage to the cell body and electro-mechanical transmission disorders; cell metabolism disorders; lesions of the cell base and electro-chemical and chemical electrical transmission disorders; and lesions of structures other than the cochlear sensory organs such as vascular striae can cause tinnitus. The pathophysiological mechanism of Ménière’s disease is recurrent chronic endolymphatic fluid accumulation. A mild increase in the pressure of the endolymphatic fluid has to be balanced by the exolymphatic fluid, and mainly at the cochlear foramen, the top of the cochlea. Displacement of the endolymphatic membrane can alter the working environment of the static cilia (static stimulation) causing turbulence at the cochlear foramen and causing higher frequency stimulation of the hair bundles. Both mechanisms increase the activity of the internal and external hair cells near the cochlear foramen and cause low frequency tinnitus. The hair cells of the basal gyrus are involved only when the disease is prolonged. Most of the sudden deafness is a cochlear lesion, and most of the tinnitus is peripheral. The majority of deafness and tinnitus produced by ototoxic drugs are also cochlear in nature. A few ototoxic drugs can cause lesions of the auditory nerve. Noise injuries can damage both the cochlea and the auditory nerve, but cochlear lesions are predominant. These diseases are often accompanied by varying degrees of hearing loss.
Clinical features:Typical cochlear tinnitus in patients with tinnitus such as Meniere’s disease is characterized by low-pitched tinnitus, typically with auditory hypersensitivity (reverberation phenomenon), and masking is effective. It is often accompanied by low-frequency hearing loss, often with auditory tonal shift.
Treatment:The principle is to reduce fluid accumulation in the inner ear. Methods include (1) low-salt diet; (2) hormone therapy, which can be considered systemic administration (oral or intravenous, 1 mg prednisone/kg body weight); tympanic chamber administration or postauricular administration; (3) diuretic therapy: such as dihydrocortisone; aminoglutethimide, etc. If the drug is used for a long time, it should be noted that hypokalemia may occur and potassium supplementation should be administered; (4) dehydration drugs: such as low molecular dextran; mannitol, etc. (5) Drugs to improve microcirculation such as betahistine; ginkgo biloba extract, etc. Endolymphatic sac decompression can be performed in early stages of Ménière’s disease. After surgery, 50% of patients feel relief from tinnitus. Positive and negative external ear canal pressure apparatus (Minette) can also be used for treatment.
Prognosis:Better.
IV. Neurogenic tinnitus.
Common diseases:Auditory neuroma; vascular collaterals compressing the auditory nerve; demyelinating lesions of the auditory nerve, etc.
Mechanism: The main cause is compression by vascular collaterals or demyelinating lesions of the nerve. Inner ear damage caused by noise or aminoglycoside ototoxic drugs is often accompanied by electrophysiological changes in the nerve fibers. The mechanism by which auditory neuroma produces tinnitus is the partial breakage of the myelin sheath of the auditory nerve fibers. Demyelination can cause a decrease in the insulation of the nerve fibers and a generalization of the auditory impulses.
Tinnitus characteristics:It is often a medium to high frequency tinnitus, and lidocaine can often reduce it. Masking therapy must be performed by selecting a sound that is at the same frequency as the tinnitus and above 20 dB above the threshold.
Treatment:Auditory neuromas require surgical treatment. Vascular collaterals compression can be surgically decompressed. It can be treated with lidocaine; carbamazepine; phenytoin sodium, etc.
Prognosis:The prognosis of acute neurogenic tinnitus is good, and it is difficult to achieve satisfactory results with chronic tinnitus medication.
V. Central tinnitus.
Common diseases:Severe central blood supply disorder p brain tumor p craniocerebral trauma p neurasthenia or post-neurosurgery can appear as central tinnitus.
Mechanism of generation:The existence of central tinnitus is not debatable. If tinnitus persists after cutting the auditory nerve, it is thought that the tinnitus comes from the auditory center. The current view is that a decrease in the function of the inhibitory neurons causes a pathological change in the spontaneous activity of the auditory nucleus causing tinnitus. It is important to note that chronic tinnitus has a “centralized” character. The pathogenesis of Ménière’s disease is water retention in the membranous vagus, and the presence of tinnitus even after vagotomy in long-standing cases suggests that the site of tinnitus is central. These phenomena are also the reasons why tinnitus should not be treated surgically.
Characteristics of tinnitus:Patients often perceive themselves as having bilateral simultaneous tinnitus, cranial tinnitus or deep head sounds that make it difficult to determine which side, masking is ineffective and lidocaine does not reduce tinnitus.
Treatment:Drug therapy for tinnitus is not effective. If the patient belongs to compensated tinnitus, it can be treated without any treatment. Regular consultation with an otolaryngologist will be sufficient. The otolaryngologist will mainly explain the mechanism of tinnitus, tell the patient to avoid strain in life, adjust the psychology, ensure the normal biological clock, and pay attention to avoid noise and ototoxic drugs. For decompensated tinnitus, drug treatment mainly focuses on the secondary decompensated symptoms, such as insomnia, anxiety, depression, etc., and provides corresponding symptomatic treatment.
Prognosis:If patients can be made to make efforts to adapt to tinnitus in order to achieve compensatory adaptation, although it is difficult to reduce the volume of tinnitus, it will not significantly affect the quality of life of patients.
VI. Tinnitus arising from extra-acoustic system.
Common diseases:It is commonly found in cervical spine dysfunction and jaw joint myoarthropathy.
Mechanism of generation:It has been found that there is a direct neural pathway connection between the cervical spinal ganglion and the auditory nucleus region of the brainstem. Therefore, cervical spine disorders may affect the auditory pathway through this neural pathway. Cervical spondylosis can cause symptoms in the ear, nose, and throat. Usually, cervical spine lesions above the third cervical vertebra often cause ear symptoms such as hearing loss, tinnitus, ear pain, and vertigo. Lesions below the fourth cervical vertebra often cause symptoms such as pharyngeal heterosensitivity, sore throat, and dysphonia. The principles of tinnitus caused by cervical spondylosis are: 1) altered spontaneous activity of neurons in the cervical spinous ganglion to the central nucleus region; 2) compression of blood vessels affecting the blood supply to the inner ear. The mechanism of tinnitus caused by jaw joint pathology is similar to that of cervical spondylosis.
Tinnitus characteristics:Tinnitus is most severe in the morning or after a nap, while other causes of tinnitus are most severe at night, when it is quiet. Another characteristic of cervical tinnitus is that the volume as well as the frequency of the tinnitus can change.
Treatment:After the cervical spine condition is relieved by treatment, about 70% of patients feel a reduction in tinnitus.
Prognosis:Better.
VII. Tinnitus caused by salicylic acid.
Large doses can cause hearing loss and induce reversible tinnitus in humans.
Mechanism: Animal tests suggest that the ABR interval is prolonged after salicylic acid use. The auditory nerve discharge is increased and can cause electrophysiological changes in the central nucleus. Nowadays, salicylic acid is often used to produce animal models of tinnitus. However, the disadvantage of this animal model is that tinnitus caused by salicylic acid intoxication is always reversible, which is not very compatible with clinical practice.
Tinnitus characteristics:Most of the tinnitus is medium-high frequency tinnitus, bilateral, and it can disappear after stopping the drug. Tinnitus symptoms usually appear only when oral doses of 400 mg or more are taken daily.
Treatment:Tinnitus usually disappears on its own after stopping salicylic acid medication.
Prognosis:Good.
VIII. Traumatic tinnitus.
Mechanism:It mostly occurs after traumatic brain injury and may be related to vagal oscillation as well as brain oscillation. The site of tinnitus can be in the cochlea, the nerve or the auditory center, or it can be mixed. There is evidence of local scarring of brain tissue in some patients with traumatic brain injury, causing abnormal discharges with the same mechanism as epilepsy.
Tinnitus features:Lidocaine can worsen tinnitus in most patients. Altered cranial pressure (both high and low cranial pressure can worsen tinnitus. In some patients, tinnitus is aggravated by the use of drugs to improve microcirculation.
Treatment:Early and adequate administration of corticosteroids to reduce brain tissue scar formation and reduce inner ear and auditory nerve edema.
Prognosis:Acute traumatic tinnitus has a good prognosis after active treatment. Chronic tinnitus has a poor prognosis.
(iii) Clinical examination and analysis.
Since tinnitus is often a concomitant symptom of systemic diseases, the root of the diagnosis and treatment of tinnitus is to clarify the cause and treat the original disease. In addition to the examination of systemic diseases, the following examinations are required.
1. Routine examination of the ear: presence of cerumen tethering in the external ear canal, presence of cerumen pieces in front of the tympanic membrane, presence of perforation of the tympanic membrane, and presence of various types of otitis media. Attention! Pre-ear tympanic cerumen fragments, hair strands or other foreign bodies can also cause tinnitus.
2. Electrical audiometry: to clarify the hearing condition, and the frequency of tinnitus can be measured at the same time. Low frequency tinnitus is mainly seen in middle and inner ear pathologies as well as cervical spondylosis.
3.Acoustic conduction: To understand the middle ear condition.
4.Auditory brainstem evoked potential: to rule out posterior cochlear lesions.
Attention! Tinnitus with hearing loss on one side requires ABR to exclude posterior cochlea pathology.
5.Otoacoustic emission: to understand the function of the outer hair cells of the cochlea.
6.Masking test: to determine the type of tinnitus as well as to help develop a treatment plan.
7.Lidocaine test: 2 mg of lidocaine per kg of body weight dissolved in 50 ml of 0. 9% saline in an IV drip for >10 minutes. Lidocaine is positive if tinnitus improves after the administration is complete. Lidocaine may not act directly on the inner ear, but mainly on the peripheral nerves. Therefore, lidocaine positive tinnitus may be referred to as “peripheral nerve tinnitus”. It can guide the future drug regimen.
8. CT and MRI examinations may be performed if necessary to exclude intracranial occupying lesions, especially in the pontine angle of the cerebellum.
9.Positron emission tomography (PET): Patients with tinnitus can show abnormal manifestations, and it is expected to be clinically applied.
(iv) Treatment.
Treatment of subjective tinnitus: The most critical thing is to try to clarify the primary cause and treat it. For tinnitus caused by cervical spondylosis, tinnitus can be relieved in 70% of patients through treatment of cervical spondylosis. However, in more clinical cases, it is impossible to find a clear cause. If the primary cause cannot be found, the treatment is carried out separately according to the following conditions
Treatment according to the course of the disease.
Acute tinnitus (duration of disease <3< span="">months): The treatment plan is the same as for sudden deafness. Treatment is given to dilate blood vessels, improve microcirculation, and nourish nerves. Also pay attention to relieving psychological stress and rest. If the ischemia is too long and has caused irreversible lesions, the drugs to improve the circulation will not be effective. This is precisely the reason why such drugs are often given clinically with poor efficacy. Commonly used regimen: low to medium frequency tinnitus is treated with hormone + microcirculation improvement (e.g. 5% glucose 250ml + ginkgo biloba 105mg + dexamethasone 10mg intravenously). High frequency tinnitus is treated with ion channel blockers + hormone therapy (0.9% saline 250ml + 2% lidocaine 10ml + dexamethasone 10mg intravenously). Corticosteroid treatment usage is recommended to be administered at 1mg/kg body weight/day. Of the 407 analyzable cases in the national multicenter study phase summary of sudden deafness with tinnitus: 369 cases (90.66% of the incidence) and with cranial tinnitus: 9 cases (2.55% of the incidence). There were 113 cured cases (28.97%), 75 effective cases (19.23%), 153 effective cases (39.23%) and 49 ineffective cases (12.56%). The total effective rate was 87.4%. This shows the importance of early treatment of acute tinnitus according to the sudden deafness protocol.
Subacute tinnitus (duration of disease between 4 months and 1 year): after the diagnosis and differential diagnosis of the primary disease, the patient is directly advised and the appropriate treatment (muscle relaxation therapy, biofeedback, autonomic training, etc.) is used to first treat diseases that can aggravate tinnitus such as cervical spondylosis, temporomandibular joint dysfunction, and to wear hearing aids as early as possible if accompanied by hearing loss. The duration and intensity of treatment depends mainly on the severity of the tinnitus. The aim is to avoid the development of chronic tinnitus, or a long-term loss of compensation. It is important to provide general information about tinnitus so that patients can manage it on their own or seek medical help when it fluctuates in the future. Treatment can be tailored to the severity of the tinnitus. Low-key tinnitus can be treated with hormone injections behind the ear.
Chronic tinnitus (disease duration > 1 year): Since the auditory center has a memory storage phenomenon for sound, the auditory stimulation generated by long-term abnormal signals in the auditory pathway can cause changes in the auditory center, so neither medication nor surgical treatment can achieve satisfactory results. Different treatment modalities have to be selected according to the patient’s tolerance of tinnitus compensations.
(1) Compensated tinnitus: It refers to those who have mild tinnitus, which can be tolerated by the patient, and who do not have neuropsychiatric symptoms such as distraction, memory loss, sleep disturbance, headache, overexcitement, depression, etc. The patient can be explained and no special treatment is needed.
(2) Loss of compensatory tinnitus: If the tinnitus is so severe that the patient cannot tolerate it and the above-mentioned series of neuropsychiatric symptoms appear, the first thing to do is to provide symptomatic treatment for the neuropsychiatric symptoms, and this type of patients should first be treated with neurasthenia or anxiety signs. Patients should also be taught to learn how to adapt to tinnitus. Most tinnitus is characterized by an increase in tinnitus in quiet situations, especially at night. During the day, it is mainly the environmental noise that plays a masking role. Therefore, tinnitus patients should avoid quiet environments as much as possible and make appropriate background noise such as soft music, Buddhist music, and the sound of water running in a goldfish bowl. Xi-sui treatment methods can be used when necessary. For those with accompanying hearing loss, hearing aids can be used for treatment. A special set of programming can be performed separately to amplify the environmental noise, which can act as a shield against tinnitus.