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With increased longevity in today’s society comes a corresponding increase in the incidence of hearing loss, dizziness and balance problems. As many as 40% of all adults will experience dizziness severe enough to warrant reporting it to their doctor. In fact, according to the National Institutes of Health, over 90 million Americans will experience dizziness or vertigo in their lifetime. Hearing loss can have many causes including aging of the auditory system, overexposure to loud noises over a period of time, infections, ear wax buildup in the ear canal, heart conditions or stroke, head injuries, tumors, certain medicines and heredity.
Common symptoms of hearing loss include being able to hear people talking, while still having difficulty understanding them, struggling to hear conversations clearly in background noise or in group situations; having difficulty hearing over the telephone or needing to turn the TV volume higher so that others complain.
Doctors of Audiology are highly trained para-medical professionals who identify, assess, and rehabilitate disorders of the auditory, vestibular, and other neural systems. We would all agree that millions of Americans are struggling to hang onto their jobs in this economy. The outer ear consists of the auricle (unlabelled), the external auditory canal, and the lateral surface of the tympanic membrane (TM). There are several other audiological tests that are also commonly abnormal in persons with conductive hearing loss. Tympanometry usually is either flat (as shown below), or shows an abnormally large volume (indicating a perforation).
Other tests that may be helpful in confirming conductive hearing loss are OAE testing and temporal bone CT scan.
Causes include a buildup of ear wax, a foreign body in the ear canal, otosclerosis, typanosclerosis (as shown above), superior canal dehiscence (which can also cause a conductive hyperacusis), external or middle ear infections (otitis externa or media), allergy with serous otitis media (fluid in middle ear), trauma to the ossicular chain such as temporal bone fracture, tumors of the middle ear such as a glomus tumor, erosion of the ossicular chain (cholesteatoma) and perforation of the tympanic membrane. A hole in the ear drum, which is called a tympanic membrane perforation, causes a conductive hearing loss.
It is generally attributed to previous ear infections or trauma (such as a tube insertion). The last step in the chain of signal transmission between sound in the air and movement of fluid in the inner ear is the middle ear. There are three small bones interposed between the large ear drum, and the small hole (oval window) across which sound is transmitted into the inner ear. Complete ossicular chain discontinuity usuall results in a large, flat conductive hearing loss.
Characteristically, hearing aids work well for conductive hearing loss, and very good hearing results can be obtained. Surgical treatment is also generally available for conductive hearing loss as it is always due to a mechanical problem.
Most surgical treatments for otosclerosis or middle ear disease involve opening of the middle ear and repair under direct vision. However, in our opinion (which is not representative of general opinion of ear surgeons), we think it is preferable to use a hearing aid until hearing becomes unservicable, and then move onto an implanted hearing aid, and skip the middle ear surgery part altogether.
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.
Studies have shown when an ear with a hearing deficit is not stimulated over time with amplification the ability to understand decreases. We are proud to have been awarded Best of Knoxville 2015 in the category of health & medicine!
Bridgewater Speech & Hearing has been recognized as one of the top Knoxville Audiology practices.
Cases that are virus positive also are positive for TNF-alpha, suggesting a possible link to autoimmune inner ear disease.
In otosclerosis, the most commonly affected portion of the bone around the inner ear (otic capsule) is the anterior oval window (about 96%). Disorders that can be mistaken for otosclerosis (a disease) include disorders of the inner ear bones (ossicles), and fluid within the middle ear. Examples of disorders of the inner ear bones other than otosclersosis include ossicular chain disruption and ossicular fixation.

In congenital ossicular fixation, the normal articulation of the small ossicular bones does not occur. Bedside: The otologic clinician should confirm audiological testing suggesting a conductive hearing loss with bedside examination.
VEMP testing can also be used to diagnose superior canal dehiscence and distinguish otosclerosis from SCD.
The symptom of paracusis Willisii, where the patient perceives speech better in a noisy background, is said to be frequently present in otosclerosis as well as other causes of conductive hearing loss. Otosclerosis does not have to be treated, as there are no medications that have been shown to work, and it will progress or not independent of any treatment. Hearing aids are effective for conductive hearing loss and certainly are less risky than having ear surgery. Lictor (2013) reviewed all medical treatments and concluded that there is no medical treatment proven to work.
At the present writing, fluoride therapy is no longer a recommended primary treatment for otosclerosis (NIH consensus), because of its effect on other bones including the possibility of increasing the risk of hip fractures.
Lippy and Berenholtz suggest adding Caltrate and 30 mg of risedronate (a biphophonate -- Actonel) in persons who do not respond to Florical and Vitamin D. The author's advice on stapedectomy (the author is not an otologic surgeon), is that the BAHA implanted hearing aid, as well as similar devices, seem better suited to treatment of otosclerosis and similar causes of conductive hearing loss than stapes surgery.
Surgery should also not be performed in patients whose hearing loss is 70 dB or less unless their speech discrimination score is 80% or better.
Riggs BL, Hodgson SF, O'Fallon WM, Chao EY, Wahner HW, Muhs JM, Cedel SL, Melton LJ 3rd.1990. Effect of fluoride treatment on the fracture rate in postmenopausal women with osteoporosis. Dizziness or vertigo is the #1 complaint of patients over the age of 70, and is the third most frequent complaint among all patients after headache and back pain.
These voids of sound are the result of some form of hearing loss, either temporary or permanent. The most common causes are related to the inner ear; therefore, referral to a Doctor of Audiology is recommended.
Audiologists provide complete diagnostic and rehabilitation services to children and adults across the entire age span. AudigyCertified™ expertise is measured by commitment to patient satisfaction, continuing education, and the expert application of current technology.
The middle ear includes the medial surface of the eardrum, the ossicular chain of bones, the eustachian tube. These can be immensely troublesome because their removal can be difficult, and infections are common. It is more accurate to say that there is a hearing reduction, as generally hearing is not greatly affected -- a 10 db drop is typical. There also seems to be a weak association with increased serum calcium (de Carvalho et al, 2006) . When these bones are fused (otosclerosis, or ossicular fixation) or broken (ossicular chain discontinuity), a conductive hearing loss is the inevitable result. When combined with a sensorineural hearing loss, this pattern may look superficially like a conductive hearing loss, because there is an air-bone gap. Persons with LVAS may develop hearing loss as well as be unusually vulnerable to inner ear disease associated with head injury.
Recently some groups (Kakehata et al, 2006) are using endoscopy for repair of ossicular chain disturbances -- in our opinion, this is still very investigational and somewhat unreasonable -- when working inside a tiny space, one needs as good an exposure as one can manage. Carhart Notch 2-kHz Bone Conduction Threshold Dip: A Nondefinitive Predictor of Stapes Fixation in Conductive Hearing Loss With Normal Tympanic Membrane.
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 hearing nerve that carries the signal to your brain atrophies, the nerve is deprived of stimulation by the deficit. By turning up the volume on a hearing device does not constitute better understanding or clarity. Although hearing loss is usually diagnosed in early adult life, the prevalence increases almost 7-fold with age (Niedermeyer et al, 2001). This may be mediated by increased activity of the renin-angiotension system (Imauchi et al, 2008). There are some differences in opinion about this - -as about 100% of monozygotic twins match up with respect to otosclerosis (Fowler, 1966).
The author's clinical experience suggests that this estimate may be an order of magnitude too high, as practically, otosclerosis is a rare diagnosis and getting rarer.
It can also involve the round window niche (30%), the internal auditory canal, and occasionally ossicles other than the stapes (Schuknecht and Kirchner 1974; Schucknecht, 1993).
The reason for this is that mistakes can be made, and when there is a significant hearing loss, inexperienced audiologists may omit or use masking incorrectly.
We have not found this to be useful and in fact find tymps to be almost universally normal (see tymps in figure towards top of this page). As mentioned above, VEMP's should be absent in conductive hearing loss, but present in sensorineural hearing loss.
The main reason for this is to exclude alternatives (such as tumors or Menieres-- otosclerosis does not protect you from other ear diseases), and also to keep in touch with the audiologist in regards to when a hearing aid might be indicated. Hearing aid technology has undergone tremendous advances since the invention of surgical treatment for otosclerosis. Monical is a preparation that is absorbed in the intestine rather than in the stomach and may cause less side effects. Note that the small end of the prosthesis is no longer adjacent to bone, and also that the entire prosthesis has rotated about 45 degrees clockwise.

If the prosthesis migrates inward, then ear drum movement may directly stimulate the saccule utricle.
This operation, which involves drilling out the bone of the mastoid, is rarely if ever offered. This may be due to increasing prevalence of measles immunization, catching up on the backlog of cases that existed before surgery was available, or just changes in how conductive hearing loss is treated.
Devices like the BAHA have less risk of dizziness or failure, and more control over the outcome. Always test each patient at least twice before doing the surgery (because mistakes can happen). We ourselves would modify this to say that acoustic reflexes should be either absent or inverted. Audiologists determine the exact needs of each individual, and then fit hearing systems such as digital hearing aids and assistive listening devices to help improve their sense of hearing. Unaddressed hearing loss has a negative impact on overall job effectiveness, opportunity for promotion and even lifelong earning power.
These are most easily removed using an examining microscope, but in some instances, surgical removal is needed. It is presently thought that persons taking calcium supplements are not at increased risk, and also that there is no risk from calcium channel blocker medications. The most common ones are cholesteatoma associated with chronic ear infection (it is not a true tumor) and glomus tumors. 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. Renin blockers (tekturna -- Aliskiren) are available, as well as many angiotension convertase inhibitors (ACE), but to our knowledge, no one has attempted their use to block worsening of otosclerosis in pregnancy.
Nuclear inclusions similar to paramyxoviral nucleocapsids have been observed in otosclerosis osteoclasts (McKenna et al, 1986; Chole and McKenna, 2001). Otosclerosis is thought to begin with otospongiosis, which is a localized softening of the normally very hard bone of the otic capsule (Shambough 1971). The malleus can be fixed at the anteior nuchal ligament, or the head can be adherent to the medial-most portion of the ear canal. Lippy and Berenholz) suggest that this condition can be diagnosed with a flat sensorineural hearing loss, good speech discrimination, absent acoustic reflexes, and a family history. It is best to confirm the conductive hearing loss both with the tuning fork test (512 hz) -- both Weber and Rinne, and with the VEMP test. This is the same patient as above (right) where the Right ear was operated, and the left ear unoperated, but both clearly had stapedial otosclerosis. This being said, it is still difficult to see the logic and we ourselves have never seen a patient who has volunteered this observation. It would seem to us, that one would need to consider both the risk of hearing progression, and balance it against the risk of adverse effects on other bones, when prescribing.
Cruise et al (2010) indicated that there is only low-quality evidence for sodium fluoride therapy being effective in otosclerosis.
If it migrates outward, a fistula can arise at the oval window, from which the prosthesis was dislodged. Because it involves creating an otic capsule fistula, similar to that seen in superior canal dehiscence, it has many untoward effects. The surgeon should be prepared, if necessary, to repair the ear drum prior to the operation, treat all infections prior to the operation, and remove exostoses at the time of the ear surgery.
Telling your Doctor when your symptoms began, when they are most likely to occur and exactly what they feel like will help your Doctor in conjunction with your Audiologist develop a more accurate diagnosis. Doctors of Audiology hold advanced degrees from accredited universities or professional schools. Practically, this is a very uncommon situation, of much more interest to diagnosticians than patients. Roughly speaking, the frequency patterns of hearing loss are divided up into: Low-frequency, mid-frequency, high-frequency, notches, and flat. This would be consistent with the observation that it is of variable penetrance, as one would expect a single gene to be more consistent in behavior. Measles virus RNA has been found in the stapes of otosclerotic persons (Potocka-Baklazek et al, 2014).
On the other hand, about 40% of stapes from otosclerosis patients are negative for measles (Karosi et al, 2007), and it is also unclear why measles should affect the temporal bone, but not affect other bones in the body. To our knowledge, nobody has yet attempted to apply this finding with anti-TNF drugs such as entanercept. There appear to be three stages of otosclerosis -resorptive osteoclastic stages with signs of inflammation, followed by an osteoblastic stage involving immature bone, followed by mature bone formation. OPH is found in high concentration in the perilymph (Zehnder et al, 2005), and thus lack of OPG might be thought of as a possible explanation for the the otospongiosis part of otosclerosis.
To us, this clinical picture would seem rather difficult to distinguish from any other type of sensorineural hearing loss. VEMP's should be absent in a conductive hearing loss but present in sensorineural hearing loss.
Another possible explanation is that persons with sensorineural hearing loss have great problems hearing in noise, perhaps because of loss of outer hair cells, but this is simply not the case in conductive hearing loss. There is not much one can do about a failed stapes procedure other than take more CT scans adding on more radiation, and then do more surgery. If you or your loved one suffer from hearing loss, vertigo or balance problems, consult your local Doctor of Audiology. As the treatments for cochlear otosclerosis vary from doing nothing to an unproven medical treatment (sodium fluoride), we would favor simply diagnosing such patients as having sensorineural hearing loss. This is called Schwartz sign -- it is not a reliable sign and should not be relied upon (Lippy and Berenholz, 2008).

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