Labyrinth lesions in infectious diseases: causes, symptoms, diagnosis, treatment

Labyrinth damage in some infectious diseases. Acute infectious diseases, especially in children, are often the cause of severe damage to the inner ear, leading to partial or complete deafness, imperfect function of the vestibular apparatus. Such diseases include epidemic cerebrospinal meningitis, epidemic mumps, influenza, a group of typhus and childhood infections, botulism, malaria, herpes, tuberculosis, syphilis, etc. Sometimes acute bilateral exclusion of the ear labyrinth occurs after a short-term infectious disease such as acute respiratory infections or influenza. An example of such an excess is Voltolini syndrome, which consists of bilateral deafness in children after a short-term acute infection that occurred without meningeal symptoms; simultaneously with the onset of deafness, it is not possible to cause excitation of the vestibular apparatus.

Epidemic cerebrospinal meningitis. Epidemic cerebrospinal meningitis is caused by meningococcus (Neisseria meningitidis). The source of infection is a patient with meningococcal nasopharyngitis, the route of transmission of the infection is airborne. The disease begins acutely with stunning chills, a rapid rise in body temperature to 38-40 ° C with a rapid deterioration in the general condition. Clinical manifestations and meningeal symptoms are typical for a severe form of meningitis. Of the cranial nerves, the optic, oculomotor, abducens, facial and vestibulocochlear are affected. Epidemic cerebrospinal meningitis in infants has a number of features: it proceeds sluggishly with weak expression or complete absence of meningeal symptoms against the background of general toxic symptoms. One of the frequent complications of epidemic cerebrospinal meningitis is meningococcal labyrinthitis, which occurs with severe vestibular symptoms with early and persistent loss of auditory function.

Treatment is carried out in hospital. In case of nasopharyngitis, rinsing the nasopharynx with a warm solution of boric acid (2%), furacilin (0.02%), potassium permanganate (0.05-0.1%) is indicated. In case of severe fever and intoxication, chloramphenicol (2 g/day for 5 days), sulfonamides or rifampicin are prescribed. In case of generalized forms of epidemic cerebrospinal meningitis and meningococcal labyrinthitis, antibiotics and hormonal drugs are used; to combat toxicosis, a sufficient amount of fluid, polyionic solutions (quartasol, trisol, rehydron), blood-substituting fluids (rheopolyglucin, hemodez) are administered. At the same time, dehydration is carried out by using diuretics (lasix, furosemide, diacarb, veroshpiron), multivitamin mixtures, antihypoxants, neuroprotectors are prescribed.

The prognosis for general recovery with timely and correct treatment is favorable, but sometimes, with generalized forms with a severe course, especially in children in the first days of life, fatal outcomes are possible. Such severe organic lesions as hydrocephalus, dementia and oligophrenia, amaurosis are extremely rare. With labyrinthitis, severe hearing loss or deafness often persists.

Epidemic parotitis. In epidemic parotitis, auditory and vestibular disorders occur quite often. The filterable virus of epidemic parotitis (Pneumophilus parotidis) affects the parenchyma of the parotid salivary gland and penetrates the meninges and cerebrospinal fluid, causing more or less pronounced phenomena of limited meningitis in the area of the MMU with the development of viral toxic-infectious neuritis of the caudal group nerves and the auditory-facial bundle located in this area. Auditory and vestibular disorders usually occur 5-10 days after the onset of the disease. They begin with increasing tinnitus and mild dizziness and can reach a high degree of severity with complete shutdown of auditory and vestibular functions on the side of the parotid salivary gland lesion.

Children aged 5-15 years are most often affected. The disease begins with a rise in body temperature to 38-39°C, slight chills, swelling and soreness of the parotid salivary gland on one side and then on the other, which is why the patient's face takes on a special appearance, which gave this disease the name "mumps". The source of the disease is a sick person from the last days of the incubation period until the 9th day of the disease. The infection is transmitted with saliva by airborne droplets. With a favorable course, auditory and vestibular disorders gradually disappear and hearing returns to normal.

Treatment is symptomatic; depending on the severity and prevalence of the viral infection, it is carried out either at home with appropriate preventive measures, or in the infectious diseases department. To prevent labyrinthine disorders, detoxification therapy, neuroprotectors, antihypoxants, antihistamines, etc. are used.

Influenza. Influenza-induced damage to the inner ear manifests itself as infectious vasculitis of its structures and the vestibulocochlear nerve. Often these lesions are accompanied by acute otitis media of influenza etiology, but they can also occur independently. The virus penetrates the inner ear hematogenously, reaches the hair cells of the vestibular apparatus, reproduces in them and causes their death. Possessing high neurotropism, the influenza virus also affects other parts of the nervous system. With influenza labyrinthitis, the same symptoms of damage to the inner ear occur as with ER, the difference is that the hearing loss that occurs with influenza remains persistent and can progress over several years.

Treatment is carried out according to the same principles as for epidemic mumps.

Typhus. Symptoms of diseases of the ear labyrinth and vestibulocochlear nerve in different forms of typhus infection have their own characteristics.

In typhus and involvement of the ear labyrinth in the infectious process, auditory and vestibular disorders appear in the first days of the disease. Vestibular symptoms are characterized by signs of labyrinth irritation (dizziness, spontaneous nystagmus towards the "causal" ear), and then its suppression. They increase, up to the period of crisis, and then disappear without any consequences. Hearing impairment with damage to the cochlea is manifested by a sharp noise in one or both ears, progressive hearing loss mainly at low frequencies, with predominant damage to the vestibulocochlear nerve, hearing loss occurs at all frequencies. The hearing impairment that occurs in typhus is of a persistent perceptual nature.

In typhoid fever, labyrinthine disorders occur 2-4 weeks after the onset of the disease, and sometimes during the recovery period. They are less pronounced than in typhus and pass without a trace. Persistent hearing impairment is rare.

In relapsing fever, hearing loss mainly occurs, sometimes accompanied by mild vestibular symptoms. Hearing loss usually develops after the second or third attack and occurs in cochlear, neuritic and mixed forms. The prognosis for hearing function is most unfavorable in the cochlear and mixed forms, in which persistent hearing loss persists, in some cases progressing over the years.

Treatment is specific anti-infective in combination with complex antineuritic therapy.

Childhood infections. Measles, scarlet fever, diphtheria, rubella and some other diseases can be complicated not only by vulgar ear infection, but also by toxic damage to its receptors, mainly the hair apparatus of the cochlea. The appearance of signs of impaired sound perception in combination with dizziness and spontaneous nystagmus with one or another childhood infection and the absence of inflammation in the middle ear indicates the involvement of the ear labyrinth and vestibular-cochlear nerve in the infectious process. For example, after diphtheria, persistent hearing loss is often observed in one or both ears with decreased excitability of one or both vestibular apparatuses, which is apparently associated with diphtheritic neuritis of the vestibular-cochlear nerve. In diphtheria, Dejerine's syndrome can sometimes be observed, caused by toxic polyneuritis, reminiscent of tabes dorsalis in its symptoms and manifested by ataxia and impaired deep sensitivity.

Rubella plays a special role in the development of irreversible labyrinthine disorders. Its virus has a high tropism for embryonic tissue, causing infection of the embryo and various malformations in the first 3 months of pregnancy. An example of such malformations is Gregg's syndrome in newborns whose mothers had rubella during the first 3 months of pregnancy (congenital cataract, retinal anomalies, optic nerve atrophy, microphthalmos, congenital nystagmus of the eyes and deafness due to underdevelopment of the inner ear structures, various malformations of the outer and middle ear, etc.). Children born with malformations of the vestibular labyrinth lag behind in physical development, are unable to learn fine locomotion and acquire sports and motor skills.

Treatment of labyrinthine dysfunctions in childhood infections is part of a complex of therapeutic measures carried out in the treatment of a specific infection, and includes antineuritic, detoxifying, antihypoxic and other types of treatment aimed at protecting the receptors of the labyrinth and the vestibulocochlear nerve from the toxic effects of infection.

Tick-borne encephalitis. This is an acute neuroviral disease that affects the gray matter of the brain and spinal cord. It manifests itself in paresis, muscle atrophy, movement disorders, intellectual impairment, and sometimes epilepsy. In the neurological stage, especially in the meningoencephalitic and poliomyelitis forms, tinnitus, speech and binaural hearing disorders are noted. Tonal hearing suffers less. Vestibular disorders are non-systemic and are caused mainly by damage to the vestibular centers, consisting of neurons that form the gray matter of nuclear formations.

Motor vestibulocerebellar disorders are masked by subcortical hyperkinesis, boulevard paralysis, flaccid paralysis of the neck and upper limb muscles. With a favorable outcome, hearing and vestibular functions are restored to normal.

Treatment is carried out in the infectious diseases department. In the first days of the disease, the administration of specific donor y-globulin, interferon and other antiviral drugs is indicated. Detoxification and dehydration therapy, administration of ascorbic acid, trental, calcium preparations are indicated; in case of pronounced signs of cerebral edema, corticosteroids are used. In case of progressive signs of respiratory failure, it is necessary to transfer the patient to artificial ventilation.

Malaria. This is an acute infectious disease caused by various types of plasmodia; it is characterized by paroxysms of fever, enlargement of the liver and spleen, and anemia. True malarial labyrinthine disorders can be observed at the height of the attack. They are manifested by noise in the ears and head, mixed-type hearing loss, unexpressed transient vestibular disorders in the form of dizziness, often non-systemic. Quinine, used to treat this disease, can cause persistent perceptual hearing loss, while the antiplasmodium drug delagyl does not have this side effect.

Shingles is caused by the Varicella-Zoster virus, which is the causative agent of chickenpox and shingles. The virus is latent in the nerve ganglia (in 95% of healthy people), and under certain unfavorable conditions (cold, intercurrent infection) it is activated and, moving along the nerve trunks to the skin, causes characteristic smallpox-like rashes along the nerve. The defeat of the auditory-facial bundle by the virus is manifested by the syndrome of herpes zoster of the ear. The signs of this syndrome are determined by the degree of involvement of the nerves of the auditory-facial bundle (auditory, vestibular, facial and intermediate). A typical form of herpes zoster of the ear is manifested by the so-called Hunt syndrome, caused by the involvement of the geniculate node in the process and includes the following clinical periods:

1. the initial period (5-7 days) is manifested by general weakness, subfebrile temperature, headache; the appearance of pain in the ear is associated with the transition of the disease to the stage of herpetic eruptions;
2. the period of herpetic eruptions is caused by a viral infection of the geniculate node and is characterized by the appearance of herpetic eruptions on the auricle, in the external auditory canal and on the eardrum, in the retroauricular region and on the soft palate along the nerve endings; herpetic eruptions are accompanied by burning pain, taste disturbances, lacrimation, hypersalivation, regional lymphadenitis;
3. a period of total peripheral paralysis of the facial nerve, occurring after the period of rashes; the paralysis is unstable, the functions of the facial nerve are restored 2-3 weeks after its damage.

The most dangerous is the so-called generalized form (the true form of herpes of the ear), in which the facial nerve paralysis is accompanied by damage to the vestibular-cochlear nerve, i.e. cochleovestibular disorders are added to Hunt's syndrome, and then this complex of symptoms is called the Sicard-Suke syndrome: severe tinnitus, perceptual hearing loss or deafness on the side of the herpetic lesion of the ear, a pronounced vestibular crisis with a rapidly occurring shutdown of the vestibular function on the affected side. Auditory and vestibular functions may be partially restored after recovery, but persistent deafness and unilateral shutdown of the vestibular apparatus often persist. Sometimes, with herpes zoster of the ear, other cranial nerves are also affected (trigeminal, oculomotor, vagus, olfactory, nerves of taste and olfactory sensitivity).

Diagnosis is not difficult with typical manifestations of Hunt syndrome, but is always difficult with dissociated clinical manifestations, for example, in the absence of facial disorders and the presence of taste sensitivity and hearing disorders. The diagnosis is established based on the presence of general infectious prodromes, typical small-vesicular rashes in the area of the outer ear and along the nerve trunks against the background of hyperemic skin, severe otalgia in the form of stabbing, burning, radiating to neighboring areas, as well as complete peripheral paralysis of the facial nerve and taste sensitivity disorder on the affected side.

Herpes zoster of the ear should be differentiated from simple herpes, banal acute external otitis, in case of sudden hearing loss and deafness - from syphilitic damage to the organ of hearing, in case of pronounced vestibular syndrome - from an attack of Meniere's disease and vestibular neuronitis. Treatment is symptomatic and etiotropic; the latter includes such modern antiviral drugs as acyclovir, famciclovir, isopropyluracil, interferon, etc.