Anatomy, Physiology, and Pathology of the Auditory, Visual, and Speech Organs - Shvetsov A.G. 2006

Auditory analyzer
Pathology of the auditory analyzer

Hearing impairment is an invisible barrier that can have far-reaching psychological and social consequences. Patients with hearing loss or complete deafness face significant difficulties. Cut off from verbal communication, they largely lose Touch with loved ones and others around them, and their behavior changes substantially. Other sensory channels are highly inadequate at performing the tasks for which hearing is responsible; therefore, hearing is the most crucial of human Senses, and its loss must not be underestimated. It is required not only for understanding the speech of others but also for The ability to speak oneself. Children deaf from birth do not learn to speak because they are deprived of auditory stimuli; thus, prelingual deafness is a particularly serious problem. The inability to speak leads to overall developmental delay, reducing learning opportunities. Therefore, children with congenital hearing impairment should start using hearing AIDS before the age of 18 months.

Children with hearing impairment are divided into three categories (Classification):

§ deaf — these are children with total hearing loss, among whom a distinction is made between deaf children without speech (early-deafened) and deaf children who have retained speech. Early-deafened children also include those with bilateral persistent hearing impairment. In children with congenital hearing impairment or hearing loss acquired before speech development, the deafness is subsequently compensated for by other analyzers (visual-spatial imagery instead of verbal-logical reasoning). The primary form of communication is facial expressions and gestures.

In children who have retained speech, it is often unclear and slurred due to the lack of auditory feedback. These children frequently develop voice disorders (inappropriate pitch, falsetto, nasality, harshness, unnatural timbre), and speech breathing disorders are also common. Psychologically, these children can be unstable, inhibited, and highly self-conscious.

§ late-deafened — children with hearing loss but relatively intact speech. They are educated in special schools using specialized curricula and appropriate educational technology to utilize residual hearing (vibrational devices, mechanical speech protection devices). Spoken language is perceived with distortions, leading to difficulties in learning, speech perception, and speech expression and articulation. These children are often withdrawn, irritable, and use language with lexical and grammatical impairments.

§ hard of hearing — these are children with partial hearing impairment that hinders auditory development, but who retain the ability to independently acquire vocabulary.

Based on the severity of hearing loss, 4 degrees are distinguished:

§ mild — perception of a whisper at a distance of 3-6 m, conversational speech at 6-8 m;

§ moderate — perception of a whisper at 1-3 m, conversational speech at 4-6 m;

§ moderately severe — perception of a whisper at 1 m, conversational speech at 2-4 m;

§ severe — perception of a whisper at no more than 5-10 cm from the ear, conversational speech at no more than 2 meters.

A decrease in hearing acuity due to pathological processes in any part of the Auditory Analyzer (hypoacusis) or hearing loss is the most common consequence of auditory analyzer pathology. Rarer forms of hearing impairment include hyperacusis, where even normal speech causes painful or unpleasant sound sensations (which can be observed in Facial Nerve lesions); double hearing (diplacusis), which occurs when the left and right ears reproduce the pitch of a sound signal differently; and paracusia — an improvement in hearing acuity in noisy environments, typical of otosclerosis.

Hypoacusis can be conventionally linked to three categories of causes:

1. Sound conduction disorders. Hearing loss due to a mechanical barrier to the passage of sound waves can be caused by the accumulation of earwax (cerumen) in the external auditory canal. It is secreted by the Glands of the external auditory canal and performs a protective function, but when it accumulates, it forms a cerumen impaction, the removal of which fully restores hearing. A similar effect is caused by the presence of Foreign bodies in the ear canal, which is particularly common in children. It should be noted that the primary danger is not so much the presence of the foreign body itself, but rather unsuccessful attempts to remove it.

Hearing impairment can be caused by a ruptured tympanic membrane due to exposure to extremely loud noises or sounds, such as a blast wave. In such cases, it is recommended to open the Mouth at the moment of the explosion. A common cause of tympanic membrane perforation is picking at the ear with hairpins, matches, or other objects, as well as unskilled attempts to remove foreign bodies from the ear. Damage to the integrity of the tympanic membrane, while other PARTS OF THE auditory organ remain intact, has a relatively minor effect on hearing function (only the perception of low-frequency sounds is affected). The main danger lies in subsequent infection and The Development of purulent inflammation in the tympanic cavity. Loss of elasticity of the tympanic membrane due to exposure to occupational noise leads to a gradual loss of hearing acuity (occupational hearing loss).

Inflammation of the tympano-ossicular system reduces its ability to amplify sound, and even with a healthy Inner ear, hearing deteriorates.

Middle ear infections (otitis media) pose a threat to hearing due to their complications, which are most frequently observed in chronic inflammation (chronic otitis media). For example, due to The formation of adhesions between the walls of the tympanic cavity and the tympanic membrane, the mobility of the latter is reduced, resulting in hearing loss and tinnitus. A very common complication of both chronic and acute purulent otitis media is perforation of the tympanic membrane. However, the main danger lies in the potential spread of inflammation to the inner ear (labyrinthitis), the Meninges (meningitis, Brain abscess), or the occurrence of systemic Blood infection (Sepsis).

In many cases, even with correct and timely Treatment, especially of chronic otitis media, full restoration of hearing function is not achieved due to scarring of the tympanic membrane and the Articulations of the auditory ossicles. Lesions of the middle ear typically cause persistent hearing loss, but complete deafness does not occur because bone conduction is preserved. Complete deafness following middle ear inflammation can only develop if the purulent process spreads from the middle ear to the inner ear.

Secondary (secretory) otitis media is a consequence of Eustachian tube obstruction due to inflammatory processes in the nasopharynx or adenoid hypertrophy. The air in the middle ear is partially absorbed by its mucous membrane, creating negative air pressure. On one hand, this limits the mobility of the tympanic membrane (resulting in hearing loss), and on the other hand, it promotes the transudation of Blood Plasma from the vessels into the tympanic cavity. The subsequent Organization OF THE plasma clot can lead to the development of adhesions in the tympanic cavity. Otosclerosis occupies a special place, characterized by the overgrowth of spongy bone, most commonly in the area of the oval window niche, which causes the stapes to become fixed in the oval window, losing its mobility. Sometimes this overgrowth can extend to the labyrinth of the inner ear, leading to impairment of both sound conduction and sound perception. It typically manifests in youth (15-16 years of age) with progressive hearing loss and tinnitus, leading to severe hearing impairment or even complete deafness.

Since middle ear lesions affect only the sound-conducting structures and do not involve the sound-perceiving neuroepithelial structures, the resulting hearing loss is called conductive. Conductive hearing loss (except for occupational) is successfully corrected in most patients through microsurgery and hearing aids.

2. Sound perception disorders. In this case, the Hair Cells of The Organ of Corti are damaged, disrupting either signal Transduction or neurotransmitter release. As a result, the transmission of information from the cochlea to the CNS is impaired, and sensory hearing loss develops.

The cause is The impact of external or internal adverse factors: childhood infectious diseases (measles, scarlet fever, epidemic cerebrospinal meningitis, mumps), systemic infections (Influenza, typhus and relapsing fever, Syphilis); drug-induced (quinine, certain Antibiotics), domestic (carbon monoxide, coal gas), and industrial (lead, mercury, manganese) intoxications; trauma; intense exposure to occupational noise and vibration; Impaired blood supply to the inner ear; atherosclerosis, and age-related changes.

Due to their deep Location within the bony labyrinth, inner ear infections (labyrinthitis) are typically complications of inflammatory processes in the middle ear or meninges, or of certain childhood infections (measles, scarlet fever, mumps). In the vast majority of cases, diffuse purulent labyrinthitis results in complete deafness due to the purulent destruction of the organ of Corti. The outcome of localized purulent labyrinthitis is partial hearing loss for specific frequencies, depending on the site of the lesion in the cochlea. In some cases of infectious diseases, it is not the microbes themselves but their toxins that penetrate the labyrinth. The dry labyrinthitis that develops in these cases proceeds without purulent inflammation and usually does not lead to the death of the neural elements of the inner ear. Therefore, complete deafness does not occur, though significant hearing loss is often observed due to the formation of scars and adhesions in the inner ear.

Hearing impairment occurs due to increased endolymphatic pressure on the sensory Cells of the inner ear, which is observed in Meniere's disease. Although the pressure increase in this condition is transient, hearing loss progresses not only during disease exacerbations but also during interictal periods.

3. Retrocochlear disorders — the inner and middle ear are healthy, but either the transmission of nerve impulses along the auditory nerve to the auditory cortex of the cerebral hemispheres or The activity of the cortical centers themselves is impaired (for example, in Brain Tumors). Lesions of the conductive pathway of the auditory analyzer can occur at any of its segments. The most common are auditory nerve neuritis, which refers to inflammatory damage not only to the auditory nerve trunk but also to the Nerve Cells that make up the spiral ganglion located in the cochlea.

Nervous Tissue is highly sensitive to any toxic influences. Therefore, a very common consequence of exposure to certain medicinal substances (quinine, arsenic, streptomycin, salicylates, aminoglycoside antibiotics, and Diuretics), toxic agents (lead, mercury, nicotine, alcohol, carbon monoxide, etc.), and Bacterial toxins is the death of the spiral ganglion Neurons. This leads to secondary descending degeneration of the hair cells of the organ of Corti and ascending degeneration of the auditory nerve fibers, resulting in complete or partial hearing loss. Notably, quinine and arsenic have the same affinity for the neural elements of the auditory organ as methyl (wood) alcohol has for the nerve endings in the eye. In such cases, hearing loss can be severe, even leading to complete deafness, and treatment is generally ineffective. Rehabilitation in these cases involves auditory training and The Use of hearing aids. Diseases of the auditory nerve trunk arise from the spread of inflammatory processes from the meninges to the nerve sheath during meningitis.

Auditory pathways in the brain can be affected by congenital anomalies as well as various brain diseases and injuries. These primarily include hemorrhages, tumors, and inflammatory brain processes (encephalitis) associated with meningitis, syphilis, etc. In all cases, such lesions are usually not isolated but are accompanied by other neurological disorders.

If the pathological process develops in one hemisphere of the brain and affects the auditory pathways below their decussation, hearing in the corresponding ear is completely or partially impaired. If it occurs above the decussation, bilateral hearing loss occurs, which is more pronounced on the side opposite to the lesion; however, complete hearing loss does not occur, as some impulses still travel along the intact Pathways of the opposite side.

Damage to the temporal lobes of the brain, where the auditory cortex is located, can occur due to cerebral hemorrhages, tumors, or encephalitis. This impairs speech comprehension, spatial localization of sound sources, and identification of their temporal characteristics. However, such lesions do not affect the ability to distinguish the frequency and intensity of sound. Unilateral cortical lesions lead to hearing loss in both ears, which is more pronounced on the contralateral side. Bilateral lesions of the pathways and the central end of the auditory analyzer are practically never observed.

Defects of the auditory Organs:

1. Aplasia — congenital complete absence or underdevelopment (for example, absence of the organ of Corti) of the inner ear.

2. Atresia — closure or narrowing of the external auditory canal; when congenital, it is usually associated with underdevelopment or complete absence of the auricle. Acquired atresia can result from prolonged inflammation of the ear canal Skin (due to chronic ear discharge) or scarring after trauma. In all cases, only complete occlusion of the auditory canal leads to significant and permanent hearing loss. In cases of incomplete occlusion, where even a minimal gap remains in the ear canal, hearing is usually unaffected.

3. Prominent ears, combined with an increase in their size — macrotia, or small size of the auricle — microtia. Since the Functional Significance of the auricle is minor, all of its diseases, injuries, and developmental anomalies, up to its complete absence, do not cause significant hearing impairment and are primarily of cosmetic importance.

4. Congenital fistulas — non-closure of the branchial cleft, opening on the anterior surface of the auricle, slightly above the tragus. The opening is barely noticeable, discharging a viscous, clear, yellowish fluid.

5. Congenital Anomalies of the middle ear — these accompany developmental Disorders of the outer and inner ear (Filling of the tympanic cavity with Bone tissue, absence of auditory ossicles, or their fusion).

The cause of congenital ear defects most often lies in disturbances during embryonic development. Such factors include pathological influences on the embryo from the maternal body (intoxication, infection, fetal trauma). Hereditary predisposition also plays a certain role.

Congenital developmental defects should be distinguished from injuries to the hearing organ that occur during childbirth. For example, even inner ear trauma can result from compression of the fetal HEAD by a narrow birth canal or the use of Obstetric Forceps during abnormal labor.

Congenital deafness or hearing impairment is either a hereditary disorder in the embryonic Development of the peripheral part of the auditory analyzer or its individual elements (outer ear, middle ear, bony labyrinth capsule, organ of Corti); hearing impairment associated with viral infections contracted by the pregnant woman in early Pregnancy (up to 3 months), such as measles, influenza, or mumps; or the consequences of toxic substances (quinine, salicylates, alcohol) entering the pregnant woman's body. Congenital hearing loss is detected as early as the first year of a child's life: they do not progress from "cooing" to pronouncing syllables or simple words, but instead gradually become completely silent. Furthermore, by the middle of the second year at the latest, a typically developing child learns to turn toward a sound stimulus. The Role of the hereditary (genetic) factor as a cause of congenital hearing disorders was somewhat exaggerated in the past. However, this factor undoubtedly carries some significance, as it is known that deaf parents are more likely to have children with congenital hearing defects than hearing parents.

Subjective reactions to noise. In addition to acoustic trauma—i.e., objectively observable hearing damage—prolonged exposure to an environment "polluted" by excessive sounds ("noise pollution") leads to increased irritability, poor Sleep, headaches, and elevated blood pressure. The discomfort caused by noise largely depends on the subject's psychological attitude toward the sound source. For instance, a resident may be annoyed by someone playing the piano two floors above, even though the volume level is objectively low and other residents have no Complaints.