Fluctuating hearing loss otitis media tratamiento,noise cancelling headphones under 200 000,infected ear piercing treatment baby - And More

Otitis media is an inflammation in the middle ear (the area behind the eardrum) that is usually associated with the buildup of fluid.
The eustachian tube, a passage between the middle ear and the back of the throat, is smaller and more nearly horizontal in children than in adults. Three tiny bones in the middle ear carry sound vibrations from the eardrum to the inner ear. If a hearing loss exists, a child does not get the full benefit of language learning experiences. Otitis media without infection presents a special problem because symptoms of pain and fever are usually not present. Genetic factors are thought to cause more than 50% of all incidents of congenital hearing loss in children (4).
In autosomal dominant hearing loss , one parent who carries the dominant gene for hearing loss and typically has a hearing loss passes it on to the child. In autosomal recessive hearing loss , both parents who typically have normal hearing, carry a recessive gene.
In X-linked hearing loss, the mother carries the recessive trait for hearing loss on the sex chromosome and passes it on to males, but not to females. There are some genetic syndromes,in which, hearing loss is one of the known characteristics. Other causes of congenital hearing loss that are not hereditary in nature include prenatal infections, illnesses, toxins consumed by the mother during pregnancy or other conditions occurring at the time of birth or shortly thereafter. Acquired hearing loss is a hearing loss which appears after birth, at any time in one's life, perhaps as a result of a disease, a condition, or an injury. Otoacoustic emissions (OAE) represents a new and very important window into the functioning of the inner ear or cochlea, the coiled structure shown in the figure below (left panel). The inner hair cells actually overlie bone in their situation in the organ of Corti (right panel) and do the main job of sending the coded information to the brain, via the nerve fibres synapsing at their base.
This figure shows an OHC which under artificial electric stimulation has changed length by about 2 µm.
The discovery that the ear can itself make sounds provided one of the first strong pieces of evidence that the outer hair cells were active cells. We can look at the corresponding frequency responses to sounds of differing pitches and achieve something that is similar to an audiogram - a plot of the outer hair cell activity versus frequency.


This method of obtaining the OAE response provides a wealth of fine detail which has proved useful in association with different kinds of ear damage. When the ear is damaged prematurely this also results in an actual loss of total number of OHC or the hair cells themselves may be damaged functionally so they can no longer perform their function of adjustment of the sensitivity of the ear.
As OAE strengths are compared across decades we see that there is a fairly rapid decline in the first 15 years of life, then it seems to plateau, then it seems to steadily decline again.
It seems we have a certain rate of ageing allowed for in the evolution of our hearing but our modern lifestyles have conspired to "use up" our excess OHC capacity much earlier than our "three score years and ten". We certainly know that maternal infection during pregnancy with such agents as rubella causes hearing loss in the unborn baby. Because OAEs are very large in neonates (see figure above), it is easy to decide whether the neonatal ear is working well or not. Otitis media is likely to block both the passage of sound into the ear and the response emitted from the hair cells coming out of the ear. The great fluctuations in the low frequency components of the emission particularly was suggestive of pressure changes occurring within the cochlea. OAE testing is also useful in patients who do not wish to or cannot respond to an audiometric test appropriately, although they have normal hearing. In people with normal hearing, if we put sound into the right ear while recording the emissions from the left ear, it brings down the size of the emissions we can record from the left ear. This is the record of a child who had a complex regime of antibiotics for chest infections including Amoxil, Septrim, Ceclor and Augmentin. Drugs such as Cisplatinum are also known to be highly ototoxic as well as being cytotoxic to tumour cells. In summary we are emphasising that there is a cocktail of effects on hair cells throughout life which are synergistically adding up to outer hair cell damage. At one extreme is a single short period of thin, clear, noninfected fluid without any pain or fever but with a slight decrease in hearing ability.
Therefore, it can be more easily blocked by conditions such as large adenoids and infections. When fluid is present, the vibrations are not transmitted efficiently and sound energy is lost. However when otitis media occurs over and over again, damage to the eardrum, the bones of the ear, or even the hearing nerve can occur and cause a permanent, sensorineural hearing loss.


It can include hereditary hearing loss or hearing loss due to other factors present either in utero (prenatal) or at the time of birth. Genetic hearing loss may be autosomal dominant, autosomal recessive, or X-linked (related to the sex chromosome). In this case there is at least a 50% probability that the child will also have a hearing loss.
Some examples are Down syndrome (abnormality on a gene), Usher syndrome (autosomal recessive), Treacher Collins syndrome (autosomal dominant), Crouzon syndrome (autosomal dominant), and Alport syndrome (X-linked). These conditions typically cause sensorineural hearing loss ranging from mild to profound in degree. Only a fraction of that movement (0.2 µm) is enough to cause the loudness of the sound to change over a 20 dB range. At the other extreme are repeated bouts with infection, thick "glue-like" fluid and possible complications such as permanent hearing loss. Until the eustachian tube changes in size and angle as the child grows, children are more susceptible to otitis media. During this time, the child may miss out on some of the information that can influence speech and language development.
The probability is higher if both parents have the dominant gene (and typically both have a hearing loss) or if both grandparents on one side of the family have hearing loss due to genetic causes.
Because both parents usually have normal hearing, and because no other family members have hearing loss, there is no prior expectation that the child may have a hearing loss. Because at least one parent usually has a hearing loss, there is prior expectation that the child may have a hearing loss. We have derived a single figure index (emission strength) representing the number of active OHC in any ear. Using this index we have been able to quickly obtain a wide range of epidemiological information never previously possible using pure tone audiometry.
1, 2, and 4 thousand Hz comparing the OAE strength to audiogram thresholds at the same range of frequencies.



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12.11.2013 admin



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