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Author: admin, 01.09.2014. Category: Ring In The Ears

This article will review basic tympanometry, measure the mobility and impedance to mobility of the tympanic membrane, and improve diagnostic accuracy during the learning curve. In some pediatric teaching programs, most residents graduate without a practical knowledge of objective tests for middle ear function. Conductive hearing loss and treatments – Conductive hearing loss is the second most common form of hearing loss. As an overview, low frequency (or tone) sensorineural hearing loss (LF SNHL or LT SNHL) is unusual, and mainly reported in Meniere's disease as well as related conditions such as low CSF pressure.
Le Prell et al (2011) suggested that low frequency hearing loss was detected in 2.7% of normal college student's ears.
Oishi et al (2010) suggested that about half of patients with LTSNHL developed high or flat hearing loss within 10 years of onset.
The new international criteria for Meniere's disease require observation of a low-tone SNHL. Gatland et al (1991) reported fluctuation in hearing at low frequencies with dialysis was common, and suggested there might be treatment induced changes in fluid or electrolyte composition of endolymph (e.g. Although OAE's are generally obliterated in patients with hearing loss > 30 dB, for any mechanism other than neural, this is not always the case in the low-tone SNHL associated with Meniere's disease. The lack of universal correspondence between audios and OAE's in low-tone SNHL in at least some patients with Meniere's, suggests that the mechanism of hearing loss may not always be due to cochlear damage. Of course, in a different clinical context, one might wonder if the patient with the discrepency between OAE and audiogram might be pretending to have hearing loss.
Papers are easy to publish about genetic hearing loss conditions, so the literature is somewhat oversupplied with these.
Bespalova et al (2001) reported that low frequency SNHL may be associated with Wolfram syndrome, an autosomal recessive genetic disorder (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness). Bramhall et al (2008) a reported that "the majority of hereditary LFSNHL is associated with heterozygous mutations in the WFS1 gene (wolframin protein).
Eckert et al(2013) suggested that cerebral white matter hyperintensities predict low frequency hearing in older adults.
Fukaya et al (1991) suggested that LFSN can be due to microinfarcts in the brainstem during surgery. Ito et al (1998) suggested that bilateral low-frequency SNHL suggested vertebrobasilar insufficiency. Yurtsever et al (2015) reported low and mid-frequency hearing loss in a single patient with Susac syndrome. There are an immense number of reports of LTSNHL after spinal anesthesia and related conditions with low CSF pressure.
Fog et al (1990) reported low frequency hearing loss in patients undergoing spinal anesthesia where a larger needle was used.
Waisted et al (1991) suggested that LFSNHL after spinal anesthesia was due to low perilymph pressure.
Wang et al reported hearing reduction after prostate surgery with spinal anesthesia (1987). We have encountered a patient, about 50 years old, with a low-tone sensorineural hearing loss that occured in the context of a herpes zoster infection (Ramsay-Hunt).
LTSNHL is generally viewed as either a variant of Meniere's disease or a variant of sudden hearing loss, and the same medications are used.


To us, this seems a little overly stringent, compared to the earlier 1995 AAO criteria that just required any kind of hearing loss, but criteria are better than no criteria. That being said, genetic conditions should not be your first thought when you encounter a patient with LTSNHL.
One would think that diabetes insipidus is so rare that hearing loss is probably not the main reason these individuals are seeking attention. These patients are extremely rare because there isn't much microsurgery done close to the brainstem. We are dubious about the conclusion of this paper because it is different than nearly every other paper in the literature.
We are dubious that this has any applicability to humans and we have never seen a patient with lithium toxicity with any LFSNHL. We have observed this occasionally ourselves, but of course, the usual pattern is a conductive hyperacusis. We find this somewhat plausible as pregnancy and delivery might be associated with spinal anesthesia, with changes in collagen, and with gigantic changes in hormonal status. The guidelines recommend using tympanometry and acoustic reflectometry to verify the presence of middle ear effusion, a sine qua non of AOM or OME. There is a large literature about genetic causes, mainly in Wolfram's syndrome ( diabetes insipidus, diabetes mellitus, optic atrophy, and deafness), probably because it is relatively easier to publish articles about genetic problems. He defined LTSNH as that the sum of the three low frequencies (125, 250, 500) was more than 100 dB, and the sum of the 3 high frequencies (2, 4, 8) was less than 60 dB. In other words, Wolfram's is probably not diagnosed mainly by ENT's or audiologists, but rather by renal medicine doctors, as DI is exceedingly rare, while LTSNHL is not so rare in hearing tests. That being said, it is very rare to encounter any substantial change in hearing after pregnancy. Pediatricians can accurately interpret tympanogram patterns and diagnose children’s middle ear infections during daily practice. Roughly speaking, the frequency patterns of hearing loss are divided up into: Low-frequency, mid-frequency, high-frequency, notches, and flat. During the performance of the test, the air pressure in the sealed ear canal is varied by means of an automatic pressure pump. This examines the range of mobility of the tympanic membrane under varying pressures, similar to the performance of pneumatic otoscopy.
The pressure pump first introduces positive pressure to +200 dePa (deca-pascals) that is quickly rarefied down to a pressure of –400 dePa over a few seconds.
The highest point in the tympanometric pattern on the y-axis is labeled as the tympanometric peak, the point of maximum admittance. This is the point where the pressure in the middle ear and the pressure in the ear canal are equal.
When there is a definable tympanometric peak, ie, no middle ear effusion, the location of the peak along the abscissa (x-axis) provides a measure of the pressure in the middle ear. The probe tip tone is directed to the tympanic membrane during the two seconds of the pressure change described above.
Sound energy is maximally absorbed into the middle ear and minimally reflected, when the air pressure on both surfaces of the tympanic membrane is equalized. The proportion of sound reflected backward toward the instrument will increase as the pressure in the middle ear falls away from the peak compliance of the TM and the TM has reduced mobility.


If there is no impedance to the transmission of sound energy such as middle ear effusion, a compliance peak pressure (peak amplitude in dePa) is shown on the graph paper.
Thus, tympanometry measures middle ear pressure by locating on the ordinate, the peak amplitude of the pressure tracing. A cord with two flexible plastic tubes exits from the instrument and ends in a metal probe tip with two holes in the end. However, infants younger than 5 or 6 months are difficult to test because of small ear canals and highly compliant canal walls. Almost all infants with Down syndrome require experience and patience and specialized equipment to obtain a valid tracing. Large clumps of earwax and squamous debris should be removed before testing, although sound is able to bypass smaller cerumen accumulations. To insert the soft probe tip, the child’s aural helix should be grasped and pulled up and backward to straighten out the ear canal and allow insertion of the soft probe tip.
When the probe tip is inserted properly and there is a hermetic seal, the automatic recording device will be triggered.
The procedure should be repeated if results are unsatisfactory or do not match findings on pneumatic otoscopy.
The wave-like pressure variation can be a bit uncomfortable for babies who move or cry, negating the test results. Realistically, a valid test can be quickly obtained for about 85% of infants in a pediatric office.
Tympanometry requires a hermetic pressure seal by the replaceable external ear tip and about 30 seconds of relative cooperation from the patient. A leak of air pressure anywhere in the system, particularly due to a poor seal between the soft probe tip and the external auditory meatus, will abort the test and create a flat line tracing. Thus, children with elliptical shaped auditory meatal openings or stenotic ear canals may not demonstrate reliable tympanogram tracings.
When there is such negative pressure, the TM is pulled medially toward the promontory of the temporal bone. AD (D=deep) tympanogram pattern occurs when the TM is very flaccid or when there is disarticulation of the ossicular chain.
If the middle ear pressure is more negative than –400 dePa, the tympanogram tracing may appear flat, even without a middle ear effusion. Any middle ear mass, including a cholesteatoma will impede transmission of sound energy and may also be associated with a flat tympanogram. There is a simple method of differentiating an occluded probe tip from a TM perforation from middle ear effusion but one should refer to the source material. Reimbursement by third party payers is reasonable, even when the procedure is used routinely to verify the diagnosis.
Most tympanometer handheld units are attached to a recording device that plugs into the wall.
Because the Welch Allyn instrument is user friendly and small, it is a reasonable choice for a private practice.



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