STUDY - Technical - New Dacian's Medicine
Hearing
disorders
(1)
Translation Draft
The perception of sounds is achieved by air and bone conduction. In aerial conduction, sound waves reach the ear by air propagation, enter the external auditory conduction, produce vibrations of the tympanic membrane, which in turn moves the hammer, anvil and stairwell. The movements of the stair leg produce pressure changes in the fluid in the inner ear, generating a wave that moves through the cochlear basilar membrane.
Bone conduction hearing occurs when the sound wave is in contact with the skull and produces vibrations of its bones, including the temporal bone, generating a wave that moves through the basilar membrane. In both cases, the motion wave moves from the base to the apex of the cochlea.
The extensions (stereocils) of the ciliated cells of the Corti organ, which are located on the basilar membrane, are in contact with the tectoria membrane and are deformed by the motion wave. There is a maximum displacement point of the basilar membrane, determined by the frequency of the stimulating tone, for each moving wave.
High-frequency tones produce maximum displacements of the basilar membrane near the base of the cochlea. As the frequency of the stimulating tone decreases, the point of maximum displacement moves towards the apex of the cochlea.
The internal and external ciliated cells of the Corti organ have different innervations, but both types of cells are mechano-receptors. The related innervation mainly reaches the internal ciliated cells, and the related innervation mainly starts from the external ciliated cells. External ciliated cells exhibit an internal organization that is somewhat similar to that of muscle fibers.
The Corti organ not only responds to acoustic stimulation, but also produces the acoustic energy that can be detected in the external auditory canal through sensitive microphones. These otoacoustic emissions (EPA) occur spontaneously and can be evoked by acoustic stimulation. The sources of this acoustic energy are represented by external ciliated cells.
The motility of external ciliated cells is determined by mechanical (acoustic) and electrical stimulation, iontophoretic ally and changes in the internal and external ion environment, being modulated by stimulating the efferent olibolochlear beam. External ciliated cells are capable of slow and rapid motility.
Slow elongations and contractions occur by increasing intracellular calcium in the presence of ATP, applying acetylcholine and changes in the ion environment (increased potassium depolarizing the cell), while rapid motility is produced by mechanical (acoustic) stimulation and continuous current stimulation.
The electrokinetic membrane is located in the outer or lateral wall of the external ciliated cells. Rapid contractile activity occurs through changes in membrane potential. Electromotility is driven by a special and probably unique generator that can achieve audible frequencies. The motility of external ciliated cells influences the micromechanics of internal ciliated cells thus achieving the cochlear amplification necessary to explain the particular sensitivity and selectivity of frequencies in the cochlea.
In the media scale and at the level of the stereociliated edge of the ciliated cells there is a continuous current rest potential, the endocohlear potential. It is generated by stria vascularis and is present whether or not there is acoustic stimulation, having an amplitude of 80 mV, which does not differ from that of intracellular potential, but its polarity is positive in the endolymph relative to the perilymph. It increases the potential difference in the stereocyllous edge of the ciliated cells, which is certainly important in transduction.
As the motion wave moves along the basilar membrane, the stereocils are deformed and several receptor potentials are produced: the microphonic cochlear potential and the positive and negative summation potentials. These receptor potentials are assumed to occur at the apical end of the stereocils. Summation potentials may be produced mainly by internal ciliated cells, and the microphonic potential of external ciliated cells.
The summation potential represents a variation in direct current that approximates the "tyre" of acoustic stimuli. The microphonic cochlear potential is an alternating current response that faithfully renders the frequency and intensity of the stimulating tone.
The current concept of cochlear transduction is that the displacement of the extremities of the stereocils causes links between the peaks of the stereocils to allow potassium to enter the cell, which leads to its depolarization. potassium causes calcium channels to open near the base, allowing calcium to enter the cell. Calcium ions stimulate the release of transmitters.
The action potential in nerve VIII occurs at 0.5 ms after the onset of microphonic cochlear potential. It is assumed that the neurotransmitter at the interface between the ciliated cells and the cochlear nerve dendritis is glutamate. Each of the cochlear nerve neurons can be activated at a frequency and intensity specific to that cell.
This phenomenon of characteristic or best frequency occurs at each level of the central auditory path: the dorsal and ventral cochlear nuclei, the trapezoid body, the upper olivar complex, the lateral wood, the lower colic, the medial genicular body and the auditory cortex.
At low frequencies, individual fibers of the auditory nerve may respond more or less in sync with the stimulating tone. At higher frequencies, a phase blockage occurs, so that neurons respond one at a time to the particular phases of the sound wave cycle. The intensity is encoded by the amplitude of the neural activity in each neuron, the number of active neurons and specific neurons that are activated.
Let's move on to hearing loss! Hearing loss may result in damage to the external auditory duct, middle ear, inner ear or central auditory tract. Injuries to the external auditory conduction or middle ear cause transmission hearing loss, while lesions of the inner ear or nerve VIII cause perception hearing loss.
Transmission hypoacusis is caused by obstruction of the external auditory conduction by wax plugs, cellular detritus and foreign bodies, inflammation of the inner wall of the conduction, stenosis and neoplasms of the conduction, perforations of the tympanic membrane, e.g. in chronic otitis media, disruption of the ossiculal chain, for example, by necrosis of the long process of the anvil through trauma or infections, fixation of osciors , such as otosclerosis, exudation, scarring or neoplasms of the middle ear.
Perception hypoacusis is mainly due to damage to the ciliated cells of the Corti organ, secondary to loud noises, viral infections, ototoxic drugs, temporal bone fractures, meningitis, cochlear otosclerosis, Meniere's disease and aging. Neural hypoacusis is mainly due to cerebellar angle tumors such as vestibular schwannoamas (acoustic neurinomas), but may also result from neoplastic, vascular, demyelinating, infectious, degenerative or trauma disease that damages the central auditory pathways.
In the case of clinical hearing evaluation, the physical examination should assess the external auditory conduction and the tympanic membrane. Careful inspection of the nose, nasopharynx and upper respiratory tract is indicated. The other cranial nerves should be carefully evaluated. Transmission hypoacusis can be differentiated from that of perception by comparing the auditory threshold by aerial conduction with that through bone conduction. Hearing testing by air conduction is performed by presenting the stimulus in the air.
Air driving hearing is affected by changes in the external auditory conduction, the efficiency of the middle ear and the integrity of the inner ear, nerve VIII and central auditory paths. Bone conduction hearing testing is performed by placing the tail of a diapazon or the oscillator of an audiometer in contact with the cranial box. Sound perception through bone conduction short-circuits the external auditory conduction and the middle ear, testing the integrity of the inner ear, nerve VIII and central auditory paths.
If the bone conduction thresholds are within normal limits, the lesion causing hearing loss is located in the external auditory conduction or in the middle ear. If both the thresholds for air and bone conduction are increased, the lesion is in the inner ear, nerve VIII or central auditory tract. Of course, transmission and perception hearing loss can coexist, in which case both the thresholds for air and bone conduction are high, but in this case the thresholds of air driving are higher than those of bone driving.
Weber and Rinne tests are used to differentiate transmission hearing loss from perception. The Weber test can be performed with a 256 or 512 Hz frequency range and the Rinne test is much more sensitive in detecting moderate transmission hearing loss if a 256 Hz dial is used.
The Weber test is performed by placing the tail of a vibrating diapazon on the vertex and asking the patient if the tone is in both ears, or better in one ear compared to the other. In the case of unilateral driving hearing-impairedness, the tone is perceived in the affected ear. In the case of a unilateral hearing-impaired perception, the tone is perceived in the unaffected ear.
The Rinne test compares the ability of sound perception pri aerial conduction with that through bone conduction. Hold the arms of a vibrating diapazon near the external auditory conduction, then place the tail of the diapazon on the mastoid process. The patient is asked to say whether the tone is perceived more strongly by air driving or by bone conduction.
In the case of transmission hearing loss, the tone is perceived as strongly, both by aerial driving and by bone conduction. In the case of perception hearing loss, both air driving and bone conduction perception are low, but air-driven stimulus is perceived as strongly as in normal hearing. The correlation of the information obtained by performing Weber and Rinne samples allows to conclude on the type of existing hearing loss, transmission or perception.
Offf, ready for today... I have way too much to run to hope I keep going... But tomorrow is a day... In which I'll move on...
The perception of sounds is achieved by air and bone conduction. In aerial conduction, sound waves reach the ear by air propagation, enter the external auditory conduction, produce vibrations of the tympanic membrane, which in turn moves the hammer, anvil and stairwell. The movements of the stair leg produce pressure changes in the fluid in the inner ear, generating a wave that moves through the cochlear basilar membrane.
Bone conduction hearing occurs when the sound wave is in contact with the skull and produces vibrations of its bones, including the temporal bone, generating a wave that moves through the basilar membrane. In both cases, the motion wave moves from the base to the apex of the cochlea.
The extensions (stereocils) of the ciliated cells of the Corti organ, which are located on the basilar membrane, are in contact with the tectoria membrane and are deformed by the motion wave. There is a maximum displacement point of the basilar membrane, determined by the frequency of the stimulating tone, for each moving wave.
High-frequency tones produce maximum displacements of the basilar membrane near the base of the cochlea. As the frequency of the stimulating tone decreases, the point of maximum displacement moves towards the apex of the cochlea.
The internal and external ciliated cells of the Corti organ have different innervations, but both types of cells are mechano-receptors. The related innervation mainly reaches the internal ciliated cells, and the related innervation mainly starts from the external ciliated cells. External ciliated cells exhibit an internal organization that is somewhat similar to that of muscle fibers.
The Corti organ not only responds to acoustic stimulation, but also produces the acoustic energy that can be detected in the external auditory canal through sensitive microphones. These otoacoustic emissions (EPA) occur spontaneously and can be evoked by acoustic stimulation. The sources of this acoustic energy are represented by external ciliated cells.
The motility of external ciliated cells is determined by mechanical (acoustic) and electrical stimulation, iontophoretic ally and changes in the internal and external ion environment, being modulated by stimulating the efferent olibolochlear beam. External ciliated cells are capable of slow and rapid motility.
Slow elongations and contractions occur by increasing intracellular calcium in the presence of ATP, applying acetylcholine and changes in the ion environment (increased potassium depolarizing the cell), while rapid motility is produced by mechanical (acoustic) stimulation and continuous current stimulation.
The electrokinetic membrane is located in the outer or lateral wall of the external ciliated cells. Rapid contractile activity occurs through changes in membrane potential. Electromotility is driven by a special and probably unique generator that can achieve audible frequencies. The motility of external ciliated cells influences the micromechanics of internal ciliated cells thus achieving the cochlear amplification necessary to explain the particular sensitivity and selectivity of frequencies in the cochlea.
In the media scale and at the level of the stereociliated edge of the ciliated cells there is a continuous current rest potential, the endocohlear potential. It is generated by stria vascularis and is present whether or not there is acoustic stimulation, having an amplitude of 80 mV, which does not differ from that of intracellular potential, but its polarity is positive in the endolymph relative to the perilymph. It increases the potential difference in the stereocyllous edge of the ciliated cells, which is certainly important in transduction.
As the motion wave moves along the basilar membrane, the stereocils are deformed and several receptor potentials are produced: the microphonic cochlear potential and the positive and negative summation potentials. These receptor potentials are assumed to occur at the apical end of the stereocils. Summation potentials may be produced mainly by internal ciliated cells, and the microphonic potential of external ciliated cells.
The summation potential represents a variation in direct current that approximates the "tyre" of acoustic stimuli. The microphonic cochlear potential is an alternating current response that faithfully renders the frequency and intensity of the stimulating tone.
The current concept of cochlear transduction is that the displacement of the extremities of the stereocils causes links between the peaks of the stereocils to allow potassium to enter the cell, which leads to its depolarization. potassium causes calcium channels to open near the base, allowing calcium to enter the cell. Calcium ions stimulate the release of transmitters.
The action potential in nerve VIII occurs at 0.5 ms after the onset of microphonic cochlear potential. It is assumed that the neurotransmitter at the interface between the ciliated cells and the cochlear nerve dendritis is glutamate. Each of the cochlear nerve neurons can be activated at a frequency and intensity specific to that cell.
This phenomenon of characteristic or best frequency occurs at each level of the central auditory path: the dorsal and ventral cochlear nuclei, the trapezoid body, the upper olivar complex, the lateral wood, the lower colic, the medial genicular body and the auditory cortex.
At low frequencies, individual fibers of the auditory nerve may respond more or less in sync with the stimulating tone. At higher frequencies, a phase blockage occurs, so that neurons respond one at a time to the particular phases of the sound wave cycle. The intensity is encoded by the amplitude of the neural activity in each neuron, the number of active neurons and specific neurons that are activated.
Let's move on to hearing loss! Hearing loss may result in damage to the external auditory duct, middle ear, inner ear or central auditory tract. Injuries to the external auditory conduction or middle ear cause transmission hearing loss, while lesions of the inner ear or nerve VIII cause perception hearing loss.
Transmission hypoacusis is caused by obstruction of the external auditory conduction by wax plugs, cellular detritus and foreign bodies, inflammation of the inner wall of the conduction, stenosis and neoplasms of the conduction, perforations of the tympanic membrane, e.g. in chronic otitis media, disruption of the ossiculal chain, for example, by necrosis of the long process of the anvil through trauma or infections, fixation of osciors , such as otosclerosis, exudation, scarring or neoplasms of the middle ear.
Perception hypoacusis is mainly due to damage to the ciliated cells of the Corti organ, secondary to loud noises, viral infections, ototoxic drugs, temporal bone fractures, meningitis, cochlear otosclerosis, Meniere's disease and aging. Neural hypoacusis is mainly due to cerebellar angle tumors such as vestibular schwannoamas (acoustic neurinomas), but may also result from neoplastic, vascular, demyelinating, infectious, degenerative or trauma disease that damages the central auditory pathways.
In the case of clinical hearing evaluation, the physical examination should assess the external auditory conduction and the tympanic membrane. Careful inspection of the nose, nasopharynx and upper respiratory tract is indicated. The other cranial nerves should be carefully evaluated. Transmission hypoacusis can be differentiated from that of perception by comparing the auditory threshold by aerial conduction with that through bone conduction. Hearing testing by air conduction is performed by presenting the stimulus in the air.
Air driving hearing is affected by changes in the external auditory conduction, the efficiency of the middle ear and the integrity of the inner ear, nerve VIII and central auditory paths. Bone conduction hearing testing is performed by placing the tail of a diapazon or the oscillator of an audiometer in contact with the cranial box. Sound perception through bone conduction short-circuits the external auditory conduction and the middle ear, testing the integrity of the inner ear, nerve VIII and central auditory paths.
If the bone conduction thresholds are within normal limits, the lesion causing hearing loss is located in the external auditory conduction or in the middle ear. If both the thresholds for air and bone conduction are increased, the lesion is in the inner ear, nerve VIII or central auditory tract. Of course, transmission and perception hearing loss can coexist, in which case both the thresholds for air and bone conduction are high, but in this case the thresholds of air driving are higher than those of bone driving.
Weber and Rinne tests are used to differentiate transmission hearing loss from perception. The Weber test can be performed with a 256 or 512 Hz frequency range and the Rinne test is much more sensitive in detecting moderate transmission hearing loss if a 256 Hz dial is used.
The Weber test is performed by placing the tail of a vibrating diapazon on the vertex and asking the patient if the tone is in both ears, or better in one ear compared to the other. In the case of unilateral driving hearing-impairedness, the tone is perceived in the affected ear. In the case of a unilateral hearing-impaired perception, the tone is perceived in the unaffected ear.
The Rinne test compares the ability of sound perception pri aerial conduction with that through bone conduction. Hold the arms of a vibrating diapazon near the external auditory conduction, then place the tail of the diapazon on the mastoid process. The patient is asked to say whether the tone is perceived more strongly by air driving or by bone conduction.
In the case of transmission hearing loss, the tone is perceived as strongly, both by aerial driving and by bone conduction. In the case of perception hearing loss, both air driving and bone conduction perception are low, but air-driven stimulus is perceived as strongly as in normal hearing. The correlation of the information obtained by performing Weber and Rinne samples allows to conclude on the type of existing hearing loss, transmission or perception.
Offf, ready for today... I have way too much to run to hope I keep going... But tomorrow is a day... In which I'll move on...
Have a good, abundant day!
Dorin, Merticaru