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Sensorineural hearing loss

Sensorineural (sound-perceptive, perceptual) hearing loss is understood to mean damage to the auditory system from the receptor to the auditory zone of the cerebral cortex. It accounts for 74% of hearing loss. Depending on the level of pathology, it is divided into receptor (peripheral), retrocochlear (radicular) and central (stem subcortical and cortical). Division is conditional. The most common is receptor hearing loss. Retrocochlear hearing loss occurs when the spiral ganglion and VIII nerve are damaged.

Etiology. Sensoneural hearing loss is a polyetiological disease. Its main causes are infections; injuries chronic cerebrovascular insufficiency; noise vibration factor; presbycusis; neuroma of the VIII nerve; radiation exposure; abnormalities of the development of the inner ear; maternal illness during pregnancy; syphilis; intoxication with certain antibiotics and medicines, salts of heavy metals (mercury, lead), phosphorus, arsenic, gasoline; endocrine diseases; alcohol and tobacco abuse.

Sensoneural hearing loss can be secondary in diseases that initially cause conductive or mixed hearing loss, and over time lead to functional and organic changes in the receptor cells of the organ of Corti. This happens with chronic suppurative otitis media, adhesive otitis media, otosclerosis and Meniere's disease.

In 20-30% of deaf and deaf-mute children, congenital deafness is noted, and in 70-80% - acquired. The cause of hearing loss in the postnatal period is a birth injury with asphyxia, impaired cerebral circulation, as well as resuscension and hemolytic jaundice.

The infectious nature of sensorineural hearing loss and deafness accounts for about 30%. In the first place are viral infections - influenza, mumps, measles, rubella, herpes, followed by epidemic cerebrospinal meningitis, syphilis, scarlet fever and typhoid.

Pathogenesis. In infectious diseases, ganglion cells, auditory nerve fibers and hair cells are affected. Meningococci and viruses are neurotropic, while other pathogens selectively act on blood vessels, while others are vaso- and neurotropic. Under the influence of infectious agents, capillary blood supply in the inner ear is disrupted and the hair cells of the main cochlear curl are damaged. Around the auditory nerve, serous fibrinous exudate with lymphocytes, neutrophils, fiber breakdown and the formation of connective tissue can form. Nervous tissue is vulnerable and within a day, the decay of the axial cylinder, myelin and upstream centers begins. A damaged nerve can partially recover. Chronic degenerative processes in the nerve trunk lead to proliferation of connective tissue and atrophy of nerve fibers.

At the heart of deafness and hearing loss in epidemic cerebrospinal meningitis is bilateral purulent labyrinthitis. The receptor, ganglion cells, the eighth nerve trunk and nucleus in the medulla are affected. After cerebrospinal meningitis, auditory and vestibular function are often lost.

With mumps, one- or two-sided labyrinthitis quickly develops or the vessels of the inner ear are affected, resulting in hearing loss, deafness with loss of vestibular function.

With influenza, a high vaso- and neurotropicity of the virus is noted. The infection spreads hematogenously and affects the hair cells, blood vessels of the inner ear. More often there is a one-sided pathology. Often, bullous-hemorrhagic or purulent otitis media develops. Damage to the organ of hearing of a viral nature is possible with herpes zoster with localization of the process in the cochlea and trunk of the VIII nerve. A violation of the auditory and vestibular functions may occur.

Thus, the pathology of the organ of hearing in infectious diseases is localized mainly in the receptor of the inner ear and auditory nerve.

In 20% of cases, the cause of sensorineural hearing loss is intoxication. Among them, the first place is occupied by ototoxic drugs: aminoglycoside antibiotics (kanamycin, neomycin, monomycin, gentamicin, biomycin, tobramycin, netilmicin, amikacin), streptomycin, tbc-statics, cytostatics (endoxan, cisplatin, etc.), analgesic drugs ), antiarrhythmic drugs (quinadine, etc.), tricyclic antidepressants, diuretics (lasix, etc.). Under the influence of ototoxic antibiotics, pathological changes occur in the receptor apparatus, vessels, especially in stria vascularis. Hair cells are initially affected in the main scroll of the cochlea, and then throughout its length. Hearing loss develops over the entire frequency spectrum, but more to high sounds. The microphone potentials of the cochlea, the promotional potential of the eighth nerve and the endolymphatic potential, that is, the resting potential, are reduced. In the endolymph, the concentration of potassium decreases and increases - sodium, hypoxia of hair cells and a decrease in acetylcholine in the labyrinth fluid. The ototoxic effect of antibiotics is observed with general and local use. Their toxicity depends on penetration through the hematolabyrinth barrier, dose, duration of use and excretory function of the kidneys. These antibiotics, especially streptomycin, affect the vestibular receptors. The ototoxic effect of antibiotics is sharply manifested in children.

Sensoneural hearing loss of vascular origin is associated with a violation of the tone of the internal carotid, vertebral arteries, circulating blood flow in the vertebral-basilar pool. This pathology leads to circulatory disorders in the spiral arteries and arteries of the vascular strip due to spasm, thrombosis, hemorrhages in the endo- and perilymphatic spaces, which is often the cause of acute deafness and hearing loss.

The traumatic origin of hearing loss includes mechanical, aku, vibro-, baro-, accelero-, electro-, actino- and chemotrauma. Mechanotrauma can cause fracture of the base of the skull, damage to the pyramid of the temporal bone, nerve VIII. Barotrauma causes rupture of the eardrum, the membrane of the round window, dislocation of the stapes and damage to the receptor cells of the organ of Corti. With prolonged exposure to high levels of noise and vibration, dystrophic changes in the receptor occur against a background of vasospasm. The neurons of the spiral ganglion and the auditory nerve are also affected. Noise and vibration primarily lead to a decrease in the perception of high and low tones, less affecting their speech area. More severe injuries are noted under the influence of high-frequency impulse noise in excess of 160 dB (at shooting ranges), which causes acute irreversible sensorineural hearing loss and deafness as a result of an acute trauma.

Presbyakusis develops due to age-related atrophy of the cochlear vessels, spiral ganglion against the background of atherosclerosis, as well as changes in the overlying parts of the auditory system. Degenerative processes in the cochlea begin already at the age of 30, but quickly progress after 50 years.

The most common causes of damage to the central parts of the auditory system are tumors, chronic cerebrovascular insufficiency, inflammatory processes of the brain, skull injuries, etc.

Syphilitic hearing loss can initially be characterized by impaired sound conduction, and then - sound perception due to pathology in the cochlea and the centers of the auditory system.

Radicular sensorineural hearing loss is accompanied by neuroma of the VIII nerve.

The progression of conductive and mixed hearing loss often leads to damage to the auditory receptor and the formation of the sensory component, and then the predominance of sensorineural hearing loss. Secondary sensorineural hearing loss in chronic suppurative otitis media, adhesive otitis media can develop over time as a result of toxic effects on the inner ear of microorganisms, inflammatory products and medications, as well as age-related changes in the hearing organ. With the cochlear form of otosclerosis, the cause of the sensorineural component of hearing loss is the spread of otosclerotic foci into the tympanic ladder, the proliferation of connective tissue in the membranous labyrinth with damage to hair cells. In Meniere's disease, conductive hearing loss passes into mixed and then sensorineural hearing loss, which is explained by progressive degenerative-dystrophic changes in the cochlea under the influence of the labyrinth hydrops, which depends on the dysfunction of the autonomic innervation of the vessels of the inner ear and biochemical disturbances in the ear lymph.

Clinic. With the course, acute, chronic forms of hearing loss are distinguished, as well as reversible, stable and progressive.

Patients complain of constant unilateral or bilateral hearing loss, which arose sharply or gradually, with progression. Hearing loss can stabilize for a long time. It is often accompanied by subjective high-frequency ear noise (squeak, whistle, etc.) from insignificant, periodic to constant and painful. Noise sometimes becomes the main concern of the patient, annoying him. With unilateral hearing loss and deafness, communication between patients and others remains normal, but with a bilateral process, it is difficult. A high degree of hearing loss and deafness lead people to isolation, loss of emotional coloring of speech and a decrease in social activity.

Patients find out the cause of hearing loss, its duration, course, nature and effectiveness of the previous treatment. An endoscopic examination of the ENT organs is carried out, the state of the auditory and vestibular functions, as well as the ventilation function of the auditory tube are determined.

The study of hearing is important for the diagnosis of sensorineural hearing loss, the level of damage to the sensory auditory tract, as well as its differential diagnosis with conductive and mixed hearing loss. With sensorineural hearing loss, whispering, as a higher frequency, is often perceived worse than conversational. The duration of tuning forks at all frequencies is reduced, but mainly at high frequencies. The lateralization of sound in Weber's experience is noted in the best-heard ear. The tuning fork experiments of Rinne, Federichi, Jelle, Bing are positive. Bone conduction in the Schwabach experiment is shortened in proportion to hearing loss. After blowing the ears, there is no improvement in hearing in whispering. The eardrum during otoscopy is not changed, its mobility is normal, the ventilation function of the auditory tube is I-II degree.

The tonal thresholds of air and bone conduction are increased. The bone-air interval is absent or does not exceed 5-10 dB in the presence of a conductive component of hearing loss. A steep drop in curves is characteristic, especially in the high-frequency zone. Clippings of tonal curves (usually bone) are noted mainly in the high-frequency region. With deep hearing loss, only islands of hearing remain at individual frequencies. In most cases, 100% speech intelligibility is not achieved with speech audiometry. The curve of the speech audiogram is shifted from the standard curve to the right and is not parallel to it. The threshold of speech sensitivity is 50 dB or more.

With the help of above-threshold tests, the phenomenon of accelerated increase in volume (FUNG) is often detected, which confirms the defeat of the Corti organ. The differential threshold of sound power (DPS) is 0.2-0.7 dB, SISI-oano - ai100%, o? Iaaiu aeneiioi? Oiie a? Iieinoe (OAA) - 95-100 aA, no? Ai aeiaie? Aneee aeaiacii neooiaiai iiey (AANI).
Auditory sensitivity to ultrasound decreases or is not perceived. Ultrasound lateralization is directed towards a better hearing ear. Speech intelligibility is reduced or lost in the midst of noise. With impedance audiometry, tympanograms are normal. Acoustic reflex thresholds increase towards high frequencies or are not detected. In the audiogram for auditory evoked potentials, the VSWR is clearly recorded, except for a wave of the first order.

Neuroma of the VIII nerve is characterized by a slow course, one-sided sensorineural hearing loss, ear noise, tonal-speech dissociation, impaired speech intelligibility against the background of noise. It is distinguished by high UDG and the absence of FUNG, the absence of lateralization of sound in Weber's experience with lateralization of ultrasound in a healthy ear. The time of reverse adaptation increases to 15 min, its threshold is shifted to 30-40 dB (normally 0-15 dB). The decay of the acoustic reflection of the stapes is noted. Normally, for 10 s the amplitude of the reflex remains constant, or decreases to 50%. The half-life of the reflex within 1.5 s is considered pathognomonic for neuroma of the VIII nerve. Stirrup reflex (ipsi and contralateral) may not be caused by stimulation of the affected side. Otoacoustic emisia (UAE) is not recorded on the affected side, the intervals between the I and V peaks of the VSWP are lengthened. There are vestibular disorders, paresis of the facial and intermediate nerves. To diagnose neurinoma of the auditory nerve, X-rays of the temporal bones are performed according to Stanvers and their tomography (conventional, computer and magnetic resonance).

With stem hearing loss, speech intelligibility is impaired, DPS is 5-6 dB (normal 1-2 dB), reverse adaptation time 5-15 minutes. (norm 5-30 s), shift of the adaptation threshold to 30-40 dB (norm 5-10 dB). As with neuroma of the YIII nerve, there is no FUNG, ultrasound is lateralized in the best-hearing ear when there is no lateralization of sound during Weber's experiment, decay of the acoustic stirrup of the stapes is noted, lengthening of the interval between I and V peaks of VSWR, UAE is not recorded on the affected side. Pathology of the brain stem at the level of the trapezoidal body leads to the loss of both contralateral reflexes of the stapes with safety - ipsilateral. Volumetric processes in the field of cross and one non-cross paths are distinguished by the absence of all reflexes, except for the ipsilateral on the healthy side.

Central hearing loss is characterized by tonal-speech dissociation, lengthening of the latent period of auditory reactions, deterioration in speech intelligibility against a background of noise, impaired spatial hearing in the horizontal plane. Binaural perception does not improve speech intelligibility. Patients often experience difficulties in perceiving radio broadcasts and telephone conversations. Afflicted with DVSP. There is a drop or lack of potentials for sounds of different tonality and intensity.

According to audiological characteristics, it is necessary to differentiate primary sensorineural hearing loss from Meniere's disease and the cochlear form of otosclerosis.

The sensorineural component of hearing loss is noted in Meniere's disease, however, positive FUNG is combined with 100% speech intelligibility and a shift in the lower boundary of perceived frequencies (UHF) to 60-80 Hz, which is typical for conductive hearing loss. SISI test is 70-100%. With asymmetric hearing, the lateralization of sound in Weber's experiment is directed to the better hearing ear, and ultrasound to the opposite ear. The fluctuating nature of hearing loss is detected by a positive glycerol test. Spatial hearing suffers in horizontal and vertical planes. Vestibular symptoms confirm the diagnosis.

The cochlear form of otosclerosis is similar to sensorineural hearing loss in the nature of the tonal audiogram, and the rest of the audiological tests indicate the conductive nature of hearing impairment (normal perception of ultrasound, UHF shift to 60-80 Hz, high UDG with wide DDS, 100% speech intelligibility at high tonal thresholds of bone conductivity.

Treatment. Distinguish treatment of acute, chronic and progressive sensorineural hearing loss. First, it aims to eliminate the cause of the disease.

Treatment of acute sensorineural hearing loss and deafness begins as early as possible, during the period of reversible changes in the nervous tissue in the order of emergency care. If the cause of acute hearing loss has not been established, then it is regarded, most often, as hearing loss of vascular origin. Recommended intravenous drip of drugs for 8-10 days - reopoliglyukin 400 ml, hemodesis 400 ml every other day; immediately after their administration, drip administration of 0.9% sodium chloride solution of 500 ml with the addition of 60 mg of prednisolone, 5 ml of 5% ascorbic acid, 4 ml of solcoseryl, 0.05 cocarboxylase, 10 ml of panangin is prescribed. The etiotropic agents for toxic sensorineural hearing loss are antidotes: unitiol (5 ml of a 5% solution intramuscularly for 20 days) and sodium thiosulfate (5-10 ml of a 30% solution intravenously 10 times), as well as an activator of tissue respiration - calcium pantothenate (20 % solution of 1-2 ml per day subcutaneously, intramuscularly or intravenously). In the treatment of acute and occupational hearing loss, hyperbaric oxygenation is used - 10 sessions of 45 minutes each. In a recompression pressure chamber, inhalation of oxygen or carbagen (depending on the spastic or paralytic form of the vascular pathology of the brain).

Pathogenetic treatment consists in the appointment of funds that provide improvement or restoration of metabolic processes and regeneration of nerve tissue. Vitamins B1, B6, A, E, cocarboxylase, ATP are used; biogenic stimulants (aloe extract, FIBS, humisole, apilak); vasodilators (nicotinic acid, papaverine, dibazole); agents that improve vascular microcirculation (trental, cavinton, stugeron); anticholinesterase agents (galantamine, proserin); agents that improve the conductivity of nerve tissue; antihistamines (diphenhydramine, tavegil, suprastin, diazolin, etc.), glucocorticoids (prednisone, dexamethasone). При показаниях назначают гипотензивные препараты и антикоагулянты (гепарин).

Применяют меатотимпанальный способ введвения лекарственных препаратов (Солдатов И.Б., 1961). Вводят галантамин с 1-2% раствором новокаина по 2 мл ежедневно до 15 инъекций на курс. Галантамин улучшает проведение импульсов в холинергических синапсах слуховой системы, а новокаин способствует уменьшению ушного шума.

Лекарственные средства (антибиотики, глюкокортикоиды, новокаин, дибазол) вводят путем заушного фонофореза или эндаурального электрофореза.

В период стабилизации тугоухости больные находятся под наблюдением врача отоларинголога, им проводят курсы превентивного поддерживающего лечения 1-2 раза в год. Для внутривенного капельного введения рекомендуется кавинтон, трентал, пирацетам. Затем внутрь назначается стугерон (циннаризин), поливитамины, биостимуляторы и антихолинэстеразные препараты. Проводится симптоматическая терапия. Эффективен энауральный электрофорез 1-5% раствора калия иодида, 0,5% раствора галантамина, 0,5% раствора прозерина, 1% раствора никотиновой кислоты.

Для уменьшения ушного шума применяют метод введения анестетиков в биологически активные точки околоушной области, а также акупунктуру, электропунктуру, электроакупунктуру, магнитопунктуру и лазеропунктуру. Наряду с рефлексотерапией проводят магнитотерапию общим солиноидом и местно аппаратом “Магнитер” eee эндауральную электростимуляцию постоянным импульсным однополярным током. При мучительном ушном шуме и неэффективностивности консервативного лечения производят резекцию барабанного сплетения.

При стойкой, длительно существующей тугоухости со стабилизацией порогов слышимости медикаментозное лечение в основном не эффективно, так как уже нарушен морфологический субстрат звуковосприятия во внутреннем ухе.

При двусторонней тугоухости или односторонней тугоухости и глухоте на другое ухо, затрудняющих речевое общение, прибегают к слухопротезированию. Слуховой аппарат обычно показан, когда величина средней потери тонального слуха на частоты 500, 1000, 2000 и 4000 Гц составляет 40-80 дБ, а разговорная речь воспринимается на расстоянии не более 1 м от ушной раковины.

В настоящее время промышленностью выпускается несколько видов слуховых аппаратов. Их основу составляют электроакустические усилители с воздушным или костным телефонами. Существуют аппараты в виде заушины, слуховых очков, карманных приемников. Современные миниатюрные аппараты с воздушным телефоном выполнены в виде ушного вкладыша. Аппараты снабжены регулятором громкости. Некоторые из них имеют устройство для подключения к телефонному аппарату. Подбор аппаратов производится в специальных слухопротезных пунктах врачом-отоларингологом-сурдологом, слухопротезистом и техником. Длительное пользование аппаратом безвредно, однако это не предотвращает прогрессирования тугоухости. При выраженной сенсоневральной тугоухости слуховые аппараты менее эфективны, чем при кондуктивной тугоухости, так как у больных сужен динамический диапазон слухового поля (ДДСП) и отмечается ФУНГ.

Социальной глухотой считается потеря тонального слуха на уровне 80 дБ и более, когда человек не воспринимает крик около ушной раковины и невозможно общение среди людей. Если слуховой аппарат неэффективен, а общение затруднено или невозможно, то человека обучают контакту с людьми с помощью мимики, жестов. Обычно это применяется у детей. Если у ребенка врожденная глухота или она развилась до овладения речью, то он является глухонемым. Состояние слуховой функции у детей выявляют как можно раньше, до трехлетнего возраста, когда реабилитация слуха и речи происходит более успешно. Для диагностики глухоты применяют не только методы субъективной аудиометрии, но, прежде всего, объективные методы – импедансную аудиометрию, аудиометрию по слуховым вызванным потенциалам и отоакустическую эмиссию. Дети с потерей слуха 70-80 дБ и отсутствием речи обучаются в школах для глухонемых, со II-III степенью тугоухости – в школах для тугоухих, а с I-II степенью тугоухости – в школах для слабослышащих. Для глухих и слабослышащих детей имеются специальные детские сады. При обучении применяется звукоусиливающая аппаратура коллективного пользования и слуховые аппараты.

В последние годы разработано и внедряется электродное слухопротезирование – хирургическая имплантация электродов в улитку практически глухих людей для электрической стимуляции слухового нерва. После операции больных обучают речевому общению.

Для профилактики сенсоневральной тугоухости проводятся мероприятия по уменьшению вредного влияния шума и вибрации, акутравмы и баротравмы на орган слуха. Применяются антифоны – ушные вкладыши, наушники, шлемофоны и др. При лечении ототоксическими антибиотиками назначают 5% раствор унитиола внутримышечно, а при развитии тугоухости эти антибиотики отменяют. Предупреждают инфекционные заболевания и другие болезни, являющиеся причиной тугоухости.

Военнослужащие с тугоухостью направляются на обследование к отоларингологу и находятся под динамическим наблюдением врача части. При показаниях производится освидетельствование по статье 40 приказа МО РФ n 315 1995 г.
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Сенсоневральная тугоухость

  1. Types of hearing loss
    The human hearing organs are complex, and hearing loss can be caused by many different reasons. There are sensorineural, conductive, mixed and genetic hearing loss. Sensorineural hearing loss (sensorineural hearing loss, cochlear neuritis, auditory nerve neuritis) is a non-infectious disease of the ear in which the auditory nerve suffers and, accordingly, sound perception. The main
  2. DIFFERENTIAL DIAGNOSTICS OF Hearing Aid
    By hearing loss is understood the difficulty of verbal communication and perception of sounds. Distinguish between conductive (sound-conducting), perceptual (sound-perceiving) and mixed types of hearing loss. The most important condition for the supply of sound energy to the hair cells of the spiral organ is the normal morphological state, the functional mobility of the sound-conducting apparatus from the outer ear to
  3. Symptoms of hearing loss
    The main symptom of sensorineural hearing loss is hearing loss. Often occurs after acute respiratory viral infections, psychoemotional stress, intoxication. Can be affected as one ear, and both at the same time. A very common symptom in this disease is noise in the ear: it can be either high-frequency (ringing, squeaking, “buzzer”, “hissing”), or low-frequency (hum). Such phenomena require immediate
  4. ПРИЧИНЫ ТУГОУХОСТИ
    The causes leading to acquired hearing loss are very diverse. Depending on which department of the organ of hearing, a pathological effect was exerted. Congenital hearing loss can be inherited as a genetic disease. У новорожденных причинами такой тугоухости являются повреждение, воздействие токсичных веществ и инфекционное заболевание, перенесенное матерью во время
  5. Sensorineural hearing loss
    Sensorineural hearing loss in the broad sense of this concept includes lesions of the sound-receiving apparatus and (or) the central part of the auditory analyzer. Most often, sensorineural hearing loss is caused by pathology of the receptor (Corti organ) and the roots of the precordial-cochlear nerve. Unilateral hearing loss and deafness are usually of peripheral origin. Distinguish between chronic, acute
  6. Sensorineural hearing loss treatment
    Sensorineural hearing loss cannot be treated surgically. In the initial stages of the disease, the diagnosis can be accurately diagnosed by intensive drug therapy in combination with physiotherapy, hyperbaric oxygenation, electrical stimulation, etc. In the case of severe sensorineural hearing loss in both ears, hearing protection is recommended as a rehabilitation - in this case
  7. Diagnosis of hearing loss
    Clarification of the function of the auditory analyzer involves mainly the implementation of topical diagnostics. The main issue of topical diagnostics is the distinction between lesions of the sound system from damage to the sound perception system. In the differential diagnosis of lesions of the auditory analyzer, the recognition of central forms of hearing loss is of particular importance. Hearing loss is treated
  8. The concept of hearing loss
    Hearing loss is a problem in the civilized world, worsening the quality of life. Impairment of auditory function is a factor leading to a lag in psychophysical development (in children) and further to social failure. Hearing pathology is one of the common causes of disability. Despite the significant success achieved in the fight against this disease, the number of suffering
  9. Rehabilitation of patients with hearing loss and deafness
    Audiology is a section of audiology that deals with the study of deafness, but in modern audiology it is often used to denote hearing impairment in the form of hearing loss. Hearing loss is such a hearing loss in which it is difficult for the patient to communicate with people using ordinary speech. In practice, deafness is a condition when a person does not perceive loud speech made near his ear.
  10. Noise loss
    Causes Working or being near woodworking equipment, chainsaws, engines, taking off or landing aircraft, using headphones to listen to music, being near speakers during concerts or discos - all this causes the destruction of hearing receptors (hair cells) in the inner ear. Any noise above 85 decibels reduces hearing. Symptoms of Nondiscrimination
  11. Hearing loss
    Причина Воспалительные процессы среднего уха (рубцы, сращения), инфекционные заболевания (корь, грипп, сифилис, скарлатина), отравления свинцом, ртутью, нерациональное использование некоторых лекарственных препаратов, черепно-мозговая травма, длительное воздействие шума, громких звуков. Тугоухость может возникать при гипертонической болезни, атеросклерозе, а также из-за нарушения кровоснабжения
  12. Методы народной медицины в лечении тугоухости
    Говоря о народных методах лечения различных заболеваний, не хочется ни в коей мере умалять значение предлагаемых рецептов и советов. Однако, начиная принимать внутрь или наружно любые аптечные препараты, мы хотя бы прочитываем аннотацию. А вот народным методам верим безоговорочно. Более того, большинство считает, что народные средства лучше использовать по принципу «чем больше, тем лучше». А ведь
  13. Otitis, hearing loss. Reasons, signs, prevention
    Otitis is an acute inflammation of the middle ear. This is a common disease in infants and toddlers. Causes. This is due to the fact that microbes easily penetrate the cavity of the middle ear through the wide and short auditory tube of the child and inflammation occurs. Signs Acute otitis media can be catarrhal and purulent. Acute catarrhal otitis media in children occurs suddenly: there is anxiety, a cry, is disturbed
  14. ЛЕЧЕНИЕ ТУГОУХОСТИ
    TREATMENT
  15. ПРОФИЛАКТИКА ТУГОУХОСТИ
    До наступления беременности Чтобы ребенок не родился с врожденным дефектом слуха, будущей маме необходимо заранее сделать прививку от коревой краснухи, уменьшив риск заболевания во время беременности. Во время беременности и родов Беременным женщинам нужно знать об опасности употребления лекарственных препаратов, воздействия химических веществ и инфекционных заболеваний для здоровья
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