Sudden deafness (hereafter referred to as sudden deafness) is a sudden onset of sensory-neural deafness of unknown origin, also known as violent deafness, first described by DeKlevn (1944), the incidence of which has been increasing year by year, with approximately 10.7 cases in 10,000 people, accounting for 2% of initial ENT cases. The incidence of both ears accounts for 4% of cases, half of which occur simultaneously in both ears, and up to 17% have been reported. There was no significant difference in the incidence between the sexes and the left and right sides. The incidence increases with age, with 3/4 of the patients being 40 years old or older at the time of the disease.
The onset and progression of the disease are rapid, and the outcome of treatment is directly related to the time of consultation. The etiology of sudden deafness is unknown, and more than 100 causes of this disease have been documented, many of which are rare. According to Mattox (1977), the causes of the disease are in the order of viral infection, vascular disease, endolymphatic edema, rupture of the vagus membrane, and a combination of these factors. Viral infections are the most common cause of the disease.
Viral infections follow the following main routes.
1. Bloodstream infection Viral particles enter the inner ear bloodstream directly from the bloodstream, causing cochlear circulation disorders or endolymphatic vaginitis.
2. The transmural route is through the subarachnoid space, through the sieve plate at the base of the internal auditory canal, or through the cochlear tubules into the ectolymphatic space, causing ectolymphatic vaginitis, so that cochlear symptoms appear after meningitis. Herpes zoster virus is the main pathogen causing ectolymphatic vaginitis.
3. Trans-circular window pathway In virus-induced non-suppurative otitis media, the infection can invade the inner ear via the circular window.
Vascular lesions are important in the pathogenesis of sudden deafness. ilson noted that the incidence of sudden deafness due to partial or total cochlear vascular occlusion is unknown, but less than viral vagotitis. It has also been suggested that vascular lesions account for 3/4 of the causes of sudden deafness. degeneration of the sensory structures of the spiral apparatus due to hypoxia as a result of vasospasm, embolism, thrombosis, vascular compression, intravascular stenosis, hemorrhage, increased blood coagulation, fluctuations in arterial blood pressure, and other vascular disorders.
The prognosis is poor in all of these cases, except for those with vasospasm, which often result in permanent deafness. The cochlear oxygen tolerance is very weak, and the cochlear microphonic potential and nerve action potential disappear after 60 s of hypoxia. If blood flow is blocked for 30 min, the cochlear potential cannot be restored, although blood flow is restored. Katsuichiro Osaki observed the phenomenon of intravascular “blockage” in cases of sudden deafness with the aid of a 55-fold magnification of the skin mucosa microscope, and concluded that this phenomenon may cause the impaired microcirculation in the inner ear and lead to sudden deafness.
The pathophysiological mechanism is pathological intravascular erythrocyte coagulation → increased blood viscosity → decreased blood flow velocity → hypoxia → increased permeability, tissue edema, blood concentration, small thrombus formation → tissue damage.
Rupture of the labyrinthine membrane refers to the rupture of the membrane of the round or oval window of the inner ear combined with the rupture of the cochlea. The rupture of the membrane causes sudden onset of sensorineural deafness, vertigo, and tinnitus. Sudden changes in middle ear air pressure and cranial pressure are caused by sudden forceful activity or a drastic change in air pressure.
The mechanism by which this change in pressure causes rupture of the vagus membrane can be understood in two ways.
1. The cerebrospinal fluid pressure increases in the exocystic pathway, and the sieve of the cochlear tubules and the internal auditory canal transmit this pressure change to the exolymphatic system, where the cochlear tubules may play a major role. Under normal circumstances, the presence of reticulocutaneous villi and barrier membranes in the cochlear tubules, so that the cerebrospinal fluid and ectolymphatic can not be unobstructed between.
2, implosion pathway Eustachian tube a tympanic chamber pressure sudden increase, pressure inward directly on the round window, or through the auditory chain act on the oval window, penetrate the round window membrane or oval window annular ligament, there is a similar inner vagus membrane (basilar membrane and vestibular membrane) rupture of the reverse chain reaction, resulting in sudden deafness.
Membrane vagal effusion some mild and moderate sudden deafness, with or without vertigo, may be a different type of Ménière’s disease. Sudden deafness may also be the first symptom of Ménière’s disease. The percentage of patients who develop Ménière’s disease last ranges from 5 to 6.6%. The tachypnea test for sudden deafness is positive in 27% (3/11 people). Tachyphylaxis is a rapid diuretic that decreases vestibular edema after application and may normalize vestibular function. The above phenomenon supports the possibility of membranous vagal effusion in some patients.
Clinical manifestations.
1. Deafness This disease is aggressive and hearing loss can occur instantaneously, within hours or days, or suddenly upon rising in the morning. In chronic cases, the deafness can gradually worsen and stop progressing only after a few days. Its degree ranges from mild to total deafness. It can be temporary or permanent. It is mostly unilateral, but occasionally occurs bilaterally or sequentially. It can be cochlear deafness or postcochlear deafness.
Tinnitus occurs before and after deafness, accounting for about 70% of cases. It usually appears a few hours before deafness, mostly as a buzzing sound, and can last for a month or more. Some patients may emphasize the tinnitus and ignore the hearing loss.
3. Vertigo about 2-5 days 1/2 sudden deafness is accompanied by varying degrees of vertigo, of which about 10% are severe deafness with nausea and vomiting, which can last 4-7 days, and mild dizziness can exist for more than 6 weeks. A small number of patients present with vertigo as the main symptom and are easily misdiagnosed as Meniere’s disease. It is relieved after several days and does not recur.
4.Ear blockage ear blockage sensation usually appears before deafness.
5. Nystagmus may be spontaneous if vertigo is present.
Examination and laboratory tests.
Detailed medical history
Patients with sudden deafness due to viral infections may provide a clear history of influenza, colds, upper respiratory infections, sore throat, paranasal sinusitis, etc., or contact with a virally infected person, which can occur weeks before the hearing loss. Patients with sudden deafness due to vascular pathology may provide a history of heart disease or hypertension, or they may have a history of diabetes, atherosclerosis, hypercholesterolemia, or other systemic disease affecting the microvascular system.
Patients with ruptured labyrinth membranes tend to have a clear history of exertion or experience of altered air pressure, such as difficult urination, defecation, coughing, sneezing, bending, laughing, etc. or swimming, diving, diving with a ventilator or underwater breathing apparatus, or unusual flight activities.
Whole body examination
The cardiovascular system, coagulation system, metabolism and immune reactivity of the body should be targeted. Neurological examination should exclude endo-aural tract and cerebellar pontocerebellar horn lesions, vertebrobasilar and cerebral vascular circulation disorders, such as taking endo-aural tract films and cervical spine films, cranial CT scans, fundus and cerebral hemograms. Some scholars have performed cerebral hemograms in 104 patients with sudden deafness and found that the cerebrovascular functional status of patients with sudden deafness is worse than that of normal subjects.
Laboratory tests
Laboratory tests include blood picture, sedimentation, clotting time, prothrombin time, platelet count, etc. Serologic tests isolate viruses and antibody titers are measured. Blood glucose, lipids, blood nitrogen and serum syphilis tests may also be considered.
Otoscopic examination of the tympanic membrane is often normal or may be slightly red.
Audiological examination pure tone audiometry air bone conduction threshold rises, usually above 50 dB. Hearing curve typing is predominantly flat, but there are also high-frequency decreasing types, high-frequency steep decreasing types, or mild low-frequency decreasing types. Suprathreshold audiometry, speech audiometry, acoustic impedance audiometry, cochlear electrograms and auditory brainstem responses are used to identify cochlear and postcochlear damage and to understand the nature, extent and dynamics of hearing loss.
Vestibular function examination
The vestibular function examination should include variable temperature test, Z nystagmus test, fistula test, Romberg test, and nystagmography if necessary. Yagi et al. reported 51 cases of sudden deafness, 50 of which had Z nystagmus on the first visit, and 38 had Z nystagmus. 48 had nystagmus electrooculography, and 30 had horizontal nystagmus. The diagnosis of sudden deafness can be made based on the above history, symptoms and various examinations. However, the etiologic diagnosis and differential diagnosis should be made as much as possible in order to provide early and reasonable treatment. In particular, it should be differentiated from pharyngeal stenosis, Ménière’s disease, and auditory neuroma.
Eustachian tube stenosis
Many patients with sudden deafness present with low-frequency hearing loss, and these patients have initial symptoms of dullness and low-pitched tinnitus, similar to eustachian tube stenosis, and complain of a feeling of lightness after ventilation; in addition, the cause of sudden deafness, a cold, is similar to eustachian tube stenosis or middle ear catarrh; if the bone conduction mask is not used correctly during the hearing examination, the patient with sudden deafness often has a conductive hearing curve. Therefore, sudden deafness can be misdiagnosed as eustachian tube stenosis and delay treatment. It should also be noted that the two diseases can occur together.
Meniere’s disease
Patients with sudden deafness often have vertigo, but it is not recurrent, and only one episode leads to terminal deafness; there are no dynamic changes in low and mid-frequency hearing thresholds; and there is a low positive rate of reverberation. Although both may have terminal vestibular disorders, sudden deafness is sometimes associated with directional exchange nystagmus, with spontaneous nystagmus seen within 3 days of onset in the fast phase of vagal excitation toward the affected side, followed by a shift to paralytic nystagmus in the fast phase toward the healthy side. Resonance is almost always present in Ménière’s disease.
Auditory neuroma
Reviewing the literature, auditory neuromas present more commonly as sudden deafness than is generally recognized. Berg reported that 17 of 133 cases of auditory neuromas presented primarily as sudden deafness, and that four recovered hearing function before auditory neuroma resection, suggesting that patients with sudden deafness, even if they recover, must be excluded from the possibility of pontocerebellar horn tumors of the cerebellum.
Hazards of sudden deafness.
1, sudden deafness can cause hearing loss: sudden deafness is a fierce disease, hearing loss can occur in an instant, or within a few hours or days. Sudden deafness in the morning when the slow deafness can gradually add up and stop only after several days of heavy.
The progression is from mild to total deafness and can be temporary or permanent, mostly unilateral and occasionally bilateral, occurring simultaneously or sequentially. It can be cochlear deafness or postcochlear deafness.
2.Sudden deafness leads to tinnitus: tinnitus occurs about 70% of the time before and after deafness. It usually appears a few hours before deafness and is mostly a buzzing sound that can last for a month or more. Some patients may emphasize tinnitus and ignore hearing loss.
3, sudden deafness leads to vertigo: vertigo about 2-5 days 1/2 sudden deafness is accompanied by varying degrees of vertigo. In about 10% for severe deafness nausea and vomiting, which can last 4-7 days. Mild dizziness can exist for more than 6 weeks. A few patients who visit the clinic with vertigo as the main symptom are easily misdiagnosed as Meniere’s disease, which remits after a few days without recurrent attacks.
4.Sudden deafness leads to ear blockage: ear blockage ear blockage feeling usually appears before deafness.
5.Sudden deafness leads to nystagmus: nystagmus can be spontaneous if vertigo exists.