Meniere's Disease Overview (Informational blog)

this is all taken from:

http://www.dizziness-and-balance.com/disorders/menieres/menieres.html

Yes, it's boring and dry, but it describes it very well and gives some background info. Next post will be more personal and answer any questions people may have.

Meniere's Disease

Timothy C. Hain, MD Page last modified: December 3, 2009

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Fig 1. Normal inner ear.

What is Meniere's disease ?

In 1861, the French physician Prosper Meniere described a condition which now bears his name. Meniere's disease is a disorder of the inner ear which causes episodes of vertigo, ringing in the ears (tinnitus), a feeling of fullness or pressure in the ear, and fluctuating hearing loss. In figure 1, the area of the ear affected is the entire labyrinth, which includes both the semicircular canals and the cochlea.

A typical attack of Meniere's disease is preceded by fullness in one ear. Hearing fluctuation or changes in tinnitus may also precede an attack. A Meniere's episode generally involves severe vertigo (spinning), imbalance, nausea and vomiting. The average attack lasts two to four hours. Following a severe attack, most people find that they are exhausted and must sleep for several hours. There is a large amount of variability in the duration of symptoms. Some people experience brief "shocks", and others have constant unsteadiness. High sensitivity to visual stimuli (visual dependence) is common. (Lacour, 1997). During the attack the eyes jump (this is called "nystagmus"). Supplemental material on the site DVD: Movie of nystagmus during a Meniere's disease attack

Fall due to otolithic crisis of Tumarkin. This is a very dangerous variant of Meniere's disease, which can result in abrupt falls.

A particularly disabling symptom is a sudden fall. These typically occur without warning. These falls are called "otolithic crisis of Tumarkin", from the original description of Tumarkin (1936). They are attributed to sudden mechanical deformation of the otolith organs (utricle and saccule), causing a sudden activation of vestibular reflexes. Patients suddenly feel that they are tilted or falling (although they may be straight), and bring about much of the rapid repositioning themselves. This is a very disabling symptom as it occurs without warning and can result in severe injury. Often destructive treatment (e.g. labyrinthectomy or vestibular nerve section) is the only way to manage this problem. Other otologic conditions also occasionally are associated with Tumarkin type falls (Black et al, 1982; Ishiyama et al, 2003). See here for more information about drop attacks.

Meniere's episodes may occur in clusters; that is, several attacks may occur within a short period of time. However, years may pass between episodes. Between the acute attacks, most people are free of symptoms or note mild imbalance and tinnitus.

Meniere's affects roughly 0.2% of the population (click here for more details about the epidemiology). Meniere's disease usually starts confined to one ear but it often extends to involve both ears over time so that after 30 years, 50% of patients with Meniere's have bilateral disease (Stahle et al, 1991). There is some controversy about this statistic however -- some authors, for example Silverstein, suggest that the prevalence of bilaterality is as low as 17% (Silverstein, 1992). We suspect that this lower statistic is due to a lower duration of follow up and that the 50% figure is more likely to be correct. Other possibilities, however, are selection bias and different patterns of the disease in different countries. Silverstein suggested that 75% of persons destined to become bilateral do so within 5 years.

In most cases, a progressive hearing loss occurs in the affected ear(s). A low-frequency sensorineural pattern is commonly found initially, but as time goes on, it usually changes into either a flat loss or a peaked pattern (click here for more information about hearing testing). Although an acute attack can be incapacitating, the disease itself is not fatal.

What causes Meniere's Disease? (Click here for a more detailed discussion)


Figure 2a: Normal membranous labyrinth	2b. Dilated membranous labyrinth in Meniere's disease (Hydrops)

The origin of Meniere's disease is presently controversial. While in the past, it was felt that plumbing problems (hydrops) in the ear were responsible for the disease, the most current opinion is that the plumbing problems are are just a marker for the Meniere's disease, rather than necessarily being responsible for the symptoms.

Traditional thinking on the origin of Meniere's disease : The most prevalent opinion is that an acute attack of Meniere's disease results from fluctuating pressure of the fluid within the inner ear. A system of membranes, called the membranous labyrinth, contains a fluid called endolymph. The membranes can become dilated like a balloon when pressure increases. This is called "hydrops". One way for this to happen is when the drainage system, called the endolymphatic duct or sac is blocked. In some cases, the endolymphatic duct may be obstructed by scar tissue, or may be narrow from birth. In some cases there may be too much fluid secreted by the stria vascularis.

Besides a stoppage up of drainage pathways, abnormally enlarged fluid pathways into the ear such as the vestibular aqueduct or cochlear aqueduct may also be associated with Meniere's like symptoms. Recent evidence is against a relationship between the cochlear aqueduct and MD (Yilmazer et al, 2001). Enlarged vestibular aqueducts are one of the most commonly identified inner ear bony malformations in children with sensorineural hearing loss of unknown cause (Oh et al, 2001). The vestibular aqueduct extends from the medial wall of the vestibule to the posterior surface of the petrous temporal bone. Most persons with enlarged vestibular aqueducts with ear disorders have hearing loss, but occasionally there is an association with vestibular problems (Shessel and Nedzelski, 1992). There may be a genetic link between enlarged vestibular aqueduct and Pendred syndrome, which is a congenital thyroid disorder.

More recent thought on the origin of Meniere's disease. On the other hand, hydrops is not found in all persons with Meniere's disease, and hydrops is also commonly found (6%) on autopsy studies of persons who had no Meniere's type symptoms (Honrubia, 1999; Rauch et al, 2001). Because Meniere's disease occurs in roughly 0.2/100 persons, and Hydrops is found in 6/100 temporal bones, there is more than an order of magnitude more people with hydrops than Meniere's disease. Thus logically, there must be something more than simply hydrops involved in the origin of Meniere's disease (see following paragraph about immunologic function as well as page on autoimmune inner ear disease).

Recently attention has also been focused on the immunologic function of the endolymphatic sac -- immune disease may contribute to a substantial percentage of Meniere's disease. We ourselves hold this opinion, based in part on a study in which patients with Meniere's disease had a very high prevalence (about 25%) of autoimmune thyroid disease (Brenner et al, 2004). On the other hand, Ruckenstein and others recently obtained a large number of autoimmune blood tests in a group of 40 patients with unilateral Meniere's disease including CBC, ANA, Anti-Sjoegren, RF, Complement, antiphospholipid antibody, western blot for heat shock protein, MHA (syphilis test), and Lyme. Only elevations in the antiphospholipid antibody test were found 27% of patients, above the expected 6-9%. anti-heat shock protein was found in 6%. They concluded that it is unlikely that autoimmune etiologies play a significant role in their population of unilateral Meniere's (Ruckenstein, 2002). Another interpretation of their data is that they may simply not have had an appropriate marker for autoimmune involvement, as well as unilateral Meniere's may have less autoimmune cause than bilateral.

Thus, the bottom line is that in most patients with Meniere's disease in 2005, the underlying cause of Meniere's disease is unknown. It is most often attributed to viral infections of the inner ear, head injury, a hereditary predisposition, and allergy.

Click here for more about the causes of Meniere's disease.

What damage is done by Meniere's Disease?

1. Hair cell death: Conventional thought is that repeated attacks of Meniere's kills hair cells in the inner ear. This is a gradual process over years, but frequently resulting in unilateral functional deafness. Cochlear (hearing) hair cells are the most sensitive. Vestibular hair cells seem more resilient but there is also a slow decline in the caloric response in the diseased ear over roughly 15 years (Stahle et al, 1991).

2. Mechanical changes to the ear. Mechanical disruption of the inner ear is also likely with dilation of the utricle and saccule of the ear being a well known pathological finding. The saccule may dilate so that in later stages, it is adherent to the underside of the stapes footplate. This mechanical disruption and distortion of normal inner ear structures may result in the gradual onset of a chronic unsteadiness, even when patients are not having attacks. The periodic dilation and shrinkage of the utricle is also a reasonable explanation for periodic attacks of another inner ear disorder, BPPV. Finally, it also seems likely that there may be rupture of the suspensory system for the membranous labyrinth. This might create some mechanical instability of the utricle and saccule and consequently some chronic unsteadiness.

There is presently no evidence that Meniere's disease kills the cochleovestibular nerve (see Kitamura et al, 1997). Thus the term "nerve deafness" is inappropriate.

How common is Meniere's disease?

Studies have shown that Meniere's disease affects about 200 out of 100,000 people (or in other words, 2/1000). This is roughly the same prevalence as multiple sclerosis (MS). The majority of people with Meniere's disease are over 40 years of age, with equal distribution between males and females. Interestingly, the Framingham study found that 2/100 people believe they have Meniere's disease in the US, suggesting that misdiagnosis is far more common than the correct diagnosis. (click here for more)

Is there a cure?

At the present time there is no cure for Meniere's disease, but there are ways to manage the condition and help control symptoms. Some recently refined treatments are rather close to a cure (i.e. low dose gentamicin). While some have suggested that Meniere's may "burn out", recent studies suggest that this is not likely (Havia and Kentala 2004)

How does the doctor know I have Meniere's disease ?


Figure 3a: Audiogram (hearing test) typical of early Meniere's disease on the right side (x=left, o=right). There is a low-tone sensorineural hearing loss.	Figure 3b: Audiogram typical of middle-stage Meniere's disease, again on the right side. Hearing is reduced at all frequencies, but more so at high and low frequencies.	Figure 3c: Audiogram typical of late-stage Meniere's disease, again on the right side. Hearing is flat, and unaidable on the right side.

Diagnosis is based on a combination of the right set of symptoms (usually episodic dizziness and hearing disturbance), hearing tests which document that hearing is reduced after an attack, and then gets better, and exclusion of alternative causes. The differential diagnosis is broad and includes perilymph fistula, recurrent labyrinthitis, migraine, congenital ear malformations of many kinds, syphilis, Lyme disease, tumors such as acoustic neuroma, multiple sclerosis, posterior fossa arachnoid cysts, and other rare entities. Symptoms similar to Meniere's (fluctuating hearing, tinnitus, vertigo) can also be caused by impending strokes in the distribution of the anterior inferior cerebellar artery (Lee and Cho, 2003). Bilaterality of hearing fluctuation suggests a vascular cause such as migraine.

The process of diagnosis usually includes hearing testing (audiometry), an ENG test, a VEMP test, several blood tests (ANA, FTA), and an MRI scan of the head. Electrocochleography (ECochG) is often helpful. As aural fullness can be caused by eustachian tube malfunction, tympanometry is sometimes useful.

Hearing tests often begin with showing a fluctuating low-frequency sensorineural hearing loss (figure 3a). Over years, this gradually progresses to a "peaked" pattern with both low and high-tone reduction (figure 3b), and finally a "flat" pattern, typically 50 db loss (110 db would be completely deaf). After about 10 years of Meniere's disease, hearing often looks like that of figure 3c, where the "peak" has become a flat sensorineural loss.

While some people have hearing that fluctuates like this without any further symptoms of dizziness or tinnitus, in most cases, this does not progress to Meniere's disease (Schaaf et al, 2001). Some recent studies have suggested that the pattern and severity of the hearing deficit does not correlate with the duration of illness (Mateijsen et al, 2001), but from our experience, it seems more likely to us that the hearing pattern is rather variable and that these authors simply did not study enough patients.

A longer discussion of the rationale for doing testing in Meniere's disease is found here.

MEDICATIONS FOR AN ACUTE ATTACK OF MENIERE'S

This is the way that we manage acute attacks at Chicago Dizziness and Hearing

Acute management Menieres

Medications commonly used for an acute attack include the following:

Meclizine (Antivert), chewable (Bonine). Dose ranges from 12.5 twice/day to 50 mg three times/day.
Lorazepam (Ativan) 0.5 mg. Usual dose is twice/day or both at the same time at onset.This medication is effective even if it is not swallowed (i.e. you can just suck on it). Tiredness is expected.
Phenergan, orally (12.5) or rectal suppository (25 mg). Usual dose is once every 12 hours as needed for vomiting.
Compazine (orally or suppository). Usual dose is 5-10 mg every 12 hours as needed for vomiting.
Zofran (orally or sublingual). Usual dose is 8mg q 12 hrs for vomiting. (this medication, sold by Glaxo, is very very expensive). Although Zofran isn't very strong, and doesn't always work, it also doesn't have much side effects either.
Decadron (dexamethasone) 4 mg orally for 4-7 days. Or a "medrol dose pack" This convenient, rapid, but not very effective treatment is gradually being replaced by steroid injections through the ear drum. It is usually an "add-on" at the time of a physicians visit for persistent symptoms (see flow chart above).

Additional information about prevention of vomiting is found here.

How do I manage an attack?

During an acute attack, lay down on a firm surface. Stay as motionless as possible, with your eyes open and fixed on a stationary object. Do not try to drink or sip water immediately, as you'd be very likely to vomit. Stay like this until the severe vertigo (spinning) passes, then get up SLOWLY. After the attack subsides, you'll probably feel very tired and need to sleep for several hours.

If vomiting persists and you are unable to take fluids for longer than 24 hours (12 hours for children), contact your doctor. He can prescribe nausea medication, and/or vestibular suppressant medication. He/she may wish to see you or even admit you to the hospital if you are dehydrated. Meclizine (Antivert), Lorazepam and Clonazepam are commonly used vestibular suppressant medications and Compazine or Phenergan are commonly used medications for nausea.

MEDICATIONS USED BETWEEN ATTACKS (also see flowchart below)

Diuretics -- those in common use all tend to be carbonic anhydrase inhibitors, or combinations, for reasons that are not entirely clear. These agents have the advantage that they may not require potassium supplementation.

Dyazide or Maxide (triamterine/HCTZ).
Moduretic(amiloride/HCTZ)
Diamox (acetazolamide)

In the United States, Dyazide (triamterine/HCTZ) is prescribed almost universally. Maxide is used when a smaller dose than found in Dyazide is needed (it is scored). Van Deelen and Huizing studied the use of diuretics in Meniere's disease in a double-blind, placebo controlled trial, and reported that it reduces vestibular complaints, but has no significant effect on hearing (1986). Thirlwall and S. Kundu (2006) were unable to come to a conclusion as to efficacy as no papers published up to 2006 were adequate for meta-analysis.

Notes: as triamterine is a folate antagonist, pregnant women should take folate supplements if not otherwise contraindicated. Occasionally persons on long-term acetazolamide develop kidney stones. All of the above have sulfa in them, which persons with sulfa allergies may be unable to tolerate. In this situation, one may try amiloride by itself, or furosemide (Lasix). Laxix should be used in low doses and with caution because it is mildly ototoxic itself.

Vestibular Suppressants (click here for more details on drug treatments)

Clonazepam(Klonapin) 0.5 mg twice a day or as needed
lorazepam (Ativan) 0.5mg twice a day or as needed
diazepam (Valium) 2 mg twice a day or as needed
meclizine (Antivert ) 12.5 mg to 25 mg as needed up to 3-4 times/day

Calcium Channel Blockers

Verapamil (Calan, Isoptin, Verelan are brand names) 120-240 mg. Sustained release should be used.
Nimodipine
Flunarizine/Cinnarizine (not available in the USA)

Steroids (commonly for severe bouts)

Dexamethasone
Prednisone
Methylprednisoline (usually in a self-tapering "dose pack").

Immune suppressants (rarely, see AIED)

Methotrexate
Steroids (see above)
Enbrel (injectable drug), Humira (injectable)

Agents that are controversial

Serc (betahistine) -- commonly used, may be placebo, but often worth trying.
Histamine injections (irrational treatment as histamine is broken down rapidly in the body).
Homeopathic treatments, such as VertigoHeel. As is the case with all homeopathic treatments, VertigoHeel is probably a placebo.
Antiviral therapy (such as acyclovir, no evidence for effectiveness)
Intratympanic dexamethasone or other steroids (becoming more common, reasonable evidence for temporary effectiveness)

What can be done to reduce the frequency and severity of Menieres disease attacks (i.e. prevention) ?

This is the way that we attempt to prevent Meniere's attacks at Chicago Dizziness and Hearing:

menieres algorithm

The purpose of treatment between attacks is to prevent or reduce the number of episodes, and to decrease the chances of further hearing loss and damage to the vestibular system. A permanent tinnitus (ringing in the ears), constant imbalance, or a progressive hearing loss may be the consequence of long-term Meniere's disease. Hearing aids may be necessary.

Standard medical treatments:

The hydrops diet regimen will probably be recommended (see following). This is an important part of treatment for virtually all patients with Meniere's disease. Experience has show that STRICT adherence to this dietary regimen will result in stabilization in most patients.
Between attacks, diuretic medication may be prescribed to help regulate the fluid pressure in the inner ear, thereby reducing the severity and frequency of the Meniere's episodes. Dyazide (a combination of triamterine and hydrochlorothiazide) is the most common medication for this purpose, and others are listed above. The literature suggests that diuretics are modestly helpful (Horner et al., 1989; Santos et al, 1993; Shinkawa and Kimura, 1986).
Vestibular suppressants such as Antivert (meclizine) or Clonazepam, and anti-emetics (e.g. phenergan) are used on an as-needed basis.

Not so standard treatments

Verapamil (typical dose: 120 SR) sometimes reduces the frequency of attacks. Nimodipine and Flunarizine have also been used. These medications are all calcium channel blockers. The evidence is not as good that these medications work. Because Menieres and Migraine are very often combined, this medication's main role may be to treat the migraine associated vertigo that can be confused with or accompany Menieres disease. This medication is especially logical if the dizzy attacks are associated with headaches.
Some physicians prescribe Histamine injections. Most physicians in the US, however, consider this treatment to be ineffective.
Prednisone or other steroids (e.g. Decadron) are occasionally helpful in short bursts. We would most often use these when considering a destructive treatment.
There are a number of new medications that do not have much of a track record that can be tried under the supervision of your doctor. There also some unusual medications which are either considered "alternative" or which are available only outside the US which might be worth considering.

What the author recommends in his practice in Chicago for medical prevention of Meniere's. These drugs are administered to most of his patients, generally in the following sequence:

Low sodium diet (1 month trial)
Salt wasting diuretic such as dyazide (1 month trial)
Verapamil 120 SR (one month trial -- dyazide is stopped)
Betahistine (2 week trial, often combined with verapamil)

These are combined with symptomatic drugs such as meclizine, benzodiazepines, and antiemetics, to be taken during attacks.

In persons with severe progressive bilateral disease, the author will generally recommend a trial of Enbrel, with the thought that in this situation an autoimmune disorder is more probable.

In persons who do not respond to this, we move on to low-dose gentamicin (see flowchart and "last resort" section), and then destructive treatment.

An emerging treatment that may eventually end up as a standard treatment is multiple injections of steroids into the middle ear.

Treatments for Meniere's that are slightly effective

(we have moved most of the (long) placebo discussion to a separate page).

The big problem with this section is separating placebo's from slightly effective treatments. This intrinsicially involves a cost-benefit comparison.

There are an immense number of placebo and probable or nearly placebo treatments for Meniere's disease. There is nothing wrong with a placebo, if it provides some benefit (presumably psychological), and you can afford to do this. However, we don't think that placebos that are billed to health care insurance providers should be supported. The treatments briefly discussed below are (probably) not placebos, but they are high in cost (because they are surgical), and low in benefit (because the literature suggests low or no efficacy).

The Meniett device's status at this writing (2006) it again seems most likely to be a slightly effective treatment. This treatment requires a surgical procedure (insertion of a ventilation tube) and purchase of a very expensive device (the pressure machine). We do not recommend Meniett treatment in our practice. We prefer low-dose gentamicin after medication fails.

Here is what a patient who had a good experience with the Meniett told me.

Last resort treatment regimens

There is a separate page on this topic, but briefly, for intractable unilateral Menieres disease cases, we often presently advise a low dose gentamicin protocol. Gentamicin is adminstered through the ear drum every month for a total of one or two administrations. We have had very good results with this procedure, and no hearing loss as yet. If this fails, then if symptoms are severe we may follow with a labyrinthectomy/BAHA combination, or in patients with good hearing and good health, vestibular neurectomy (see "well accepted surgical treatment section above).

Persons who have intractable bilateral Meniere's disease are offered a trial of steroids with a safer immunosuppressant should this be effective, a modified gentamicin protocol, and very occasionally systemic aminoglycosides do deaden both ears.

In our opinion, medical treatments, including a reasonable trial of anti-migraine drugs, should precede use of any last resort treatment.

Pregnancy and Menieres

Pregnancy is thought to have no net effect on Meniere's disease. The difficulty in pregancy is that there should be an effort to avoid medications that might cause birth defects or otherwise injure the unborn child.

In persons who are unfortunate enough to have a flare during pregnancy, we attempt to manage them with salt restriction, minimal use of meclizine. In persons with severe symptoms, we suggest use of intratympanic steroids (dexamethasone).

How might Meniere's disease affect my life?

Meniere's disease has a severe impact on people's lives. In acute episodes, Meniere's disease is one of the most debilitating disease experienced by people who survive any illness (Anderson and Harris, 2001). Meniere's may persist for 20 years or more. It is generally a chronic disease (Havia et al, 2004).

Since the acute symptoms of Meniere's disease are episodic, it is important to explain to your family and friends what might happen when you have an attack. Then, if the symptoms occur when they are present, they will understand and not be overly frightened.

You may be able to protect yourself from injury if you feel that an attack is about to begin. Some attacks may occur during the night, so be sure you have a night light on; you'll be relying more on vision to help maintain your balance. You will want to make sure that the path to the bathroom is free of throw rugs, furniture or other obstructions.

Many studies have documented that patients with Meniere's disease tend to have more psychological disability than the normal population, possibly including depression and/or anxiety. This is generally a reaction to their disease (Savastano et al, 2007). It may be necessary to take antidepressants or anti-anxiety drugs, under the supervision of an appropriate health care professional.

Hydrops Diet (see here for more detail)

The fluid-filled hearing and balance structures of the inner ear normally function independent of the body's overall fluid/blood system. In a normal inner ear, the fluid is maintained at a constant volume and contains specific concentrations of sodium, potassium, chloride and other electrolytes. This fluid bathes the sensory cells of the inner ear and allows them to function normally.

With injury or degeneration of the inner ear structures, independent control is lost, and the volume and concentration of the inner ear fluid fluctuates with changes in the body's fluid/blood. This fluctuation causes the symptoms of hydrops--pressure or fullness in the ears, tinnitus (ringing in the ears), hearing loss, dizziness and imbalance.

Note that it is not the overall level of sodium that is important, but whether or not it fluctuates. It is not necessary or wise to lower your salt intake to amounts barely able to sustain life. We do not encourage use of 1 gram sodium diets. Rather the goal is to keep sodium levels from fluctuation. A 2 gram diet is usually possible.

More information on Meniere's disease:

Self-help groups.

The EAR Foundation (2000 Church Street, Box 111, Nashville, TN 37236)
Self-Help for Hard of Hearing (7800 Wisconsin Ave, Bethesda, MD 20814).
Vestibular Disorder Association (VEDA) P.O. Box 4467, Portland Oregon 972008-4467

References:

Anderson JP, Harris JP. Impact of Meniere's disease on quality of life. Otol Neurotol 22:888-894,2001
Black, F. O., M. Z. Effron and D. S. Burns (1982). "Diagnosis and management of drop attacks of vestibular origin: Tumarkin's otolithic crisis." Otolaryngol Head Neck Surg90(2): 256-62.
Brenner M, Hoistad D, Hain TC. Prevalence of thyroid dysfunction in Meniere's Disease. Archives of Oto HNS, 130/2 226-228 (2004)
Franz P, Hamzavi JS, Schneider B, Ehrenberger K.Do middle ear muscles trigger attacks of Meniere's disease? Acta Otolaryngol 2003 Jan;123(2):133-7

HAVIA M, Kentala E. Progression of symptoms of dizziness in Meniere's disease. Arch Otolaryngol Head Neck Surg 2004;130:431-5.
Honrubia V. Pathophysiology of Meniere's disease. Meniere's Disease (Ed. Harris JP) 231-260, 1999, Pub: Kugler (The Hague)
Horner, K. C., C. Aurousseau, et al. (1989). "Long-term treatment with chlorthalidone reduces experimental hydrops but does not prevent the hearing loss." Acta Otolaryngol 108(3-4): 175-83.
Gail Ishiyama, MD; Akira Ishiyama, MD; Robert W. Baloh, MD. Drop Attacks and Vertigo Secondary to a Non-Meniere Otologic Cause. Arch Neurol, 2003
Kinney SE, Sandridge SA, Newman CW. Long-term effects of Meniere's disease on hearing and quality of life. Am J Otol 1997 Jan;18(1):67-73.
Kitamura K, Kaminga C, Ishida T, Silverstein H. Ultrastructural analysis of the vestibular nerve in Meniere's disease. Auris Nasus Larynx 1997;24(1):27-30.
Lacour M, and others. sensory strategies in human postural control before and after unilateral vestibular neurotomy. Experimental Brain Research (2) 300-10, 1997.
Lee H, Cho YW. Auditory disturbance as a prodrome of anterior inferior cerebellar artery infarction. J. Neurol Neurosurg Psych 2003:74:1644-1648
Maier and others. Middle ear pressure and dysfunction of the labyrinth: is there a relationship ? Annals of ORL 106(6): 478-82, 1997
MATEIJSEN DJ, Van Hengel PW, Van Huffelen WM, Wit HP, Albers FW. Pure-tone and speech audiometry in patients with Meniere's disease. Clin Otolaryngol 2001; 26: 379-87.
Oh A, Ishiyama A, Baloh RB. Vertigo and the enlarged vestibular aqueduct syndrome. J. Neurol 248:971-974, 2001
Rauch SD, Merchant SN, Thediner BA. Meniere's syndrome and endolymphatic hydrops: double blind temporal bone study. Ann ORL 98(11):873-883, 1989
Ruckenstein MJ and others. Immunologic and serologic testing in patients with Meniere's disease. Otol Neurotl 23:517-521, 2002
Santos, P. M., R. A. Hall, et al. (1993). "Diuretic and diet effect on Meniere's disease evaluated by the 1985 Committee on Hearing and Equilibrium guidelines." Otolaryngol Head Neck Surg 109(4): 680-9.
Savastino M, Marioni G, Aita M. Psychological characteristics of patients with Meniere's disease compared with patients with vertigo, tinnitus or hearing loss. ENT journal, 148-156, 2007
Savastano M, Maron MB, Mangialaio M, Longhi P, Rizzardo R. Illness behavior, personality traits, anxiety and depression in patients with Meniere's disease. J Otolaryngol 1996 Oct;25(5):329-333.
Schessel DA, Nedzelski JM. Presentation of large vestibular aqueduct syndrome to a dizziness unit. J. Otolaryngol 21:265-269, 1992
Selivanova, O. A., H. Gouveris, A. Victor, et al. (2005). "Intratympanic dexamethasone and hyaluronic acid in patients with low-frequency and Meniere's-associated sudden sensorineural hearing loss." Otol Neurotol26(5): 890-5.
Selmani et al. Use of electrocochleography for assessing endolymphatic hydrops with Lyme Disease and Meniere's disease. Acta Otolaryngol 122(2) 173-8, 2002
SCHAAF H, Seling B, Rienhoff NK, Laubert A, Nelting M, Hesse G. [Is recurrent loss of low frequency tone perception--without vertigo--a precursor of Meniere disease?] HNO 2001; 49: 543-7.
Shinkawa, H. and R. S. Kimura (1986). "Effect of diuretics on endolymphatic hydrops." Acta Otolaryngol 101(1-2): 43-52.
Stahle J, Friberg U, Svedberg A. Long-term progression of Meniere's disease. Acta Otolaryngol (Stockh) 1991:Suppl 485:75-83
Thirlwall, A. S. and S. Kundu (2006). "Diuretics for Meniere's disease or syndrome." Cochrane Database Syst Rev 3: CD003599.
Torok N (1977). "Old and new in Meniere disease." Laryngoscope 87(11): 1870-7.
Tumarkin A. The otolithic catastrophe: a new syndrome. Br. Med J. 1936:1:175-177
van Deelen, G. W. and E. H. Huizing (1986). "Use of a diuretic (Dyazide) in the treatment of Meniere's disease. A double-blind cross-over placebo-controlled study." ORL J Otorhinolaryngol Relat Spec 48(5): 287-92.
Yilmazer C. Relationship of the cochlear aqueduct and inner ear pressure in Meniere's disease and in a normal population. Otol Neurotol 22: 534-538, 2001

Books on Meniere's Disease:

Meniere's Disease : What you need to know by P.J. Haybach, Jerry Underwood (This book was written under the auspices of VEDA (Vestibular Disorder Association) for patients).

Labels: balance, dizzy, ear, Meniere's Disease, nausea, vertigo

Changes, Changes, Changes

Well, clearly there are going to be changes since my last post (don't judge!), however, there have also been changes as of late that are just as notable. :)

I am now working as a Data Manager/Counselor Intern for Reno-Sparks Tribal Health Center's Intensive Outpatient Program. Quite a mouthful huh? In a nutshell, I basically interview Drug Court clients who come in for substance abuse issues and compile their data to send to the Feds for our grant reporting. Also, since I was a substance abuse counselor in the past, I'm currently interning again and preparing for the Licensing exam, which will most likely be sometime in December. I am so much happier in my job, it isn't even funny. I don't have that constant pit in my stomach the moment I drive into the parking lot. I don't dread Sundays because that means Monday is right around the corner. I don't burst into tears due to stress and unhappiness. I think now I can breathe a huge sigh of relief. Ahhhhhh.

Another new (and much anticipated) change is my new car! I previously had a trusty old Honda Civic, but recently upgraded to a Ford Escape (which I LOOOVE). It's so nice to have 4 doors! haha. Sometimes I miss zipping around in my 'ol Civic (RIP), but I absolutely love my new car.

Last, but not least, I finally chopped my hair off. I haven't had hair this short since early grade school, but it was definitely time. I told my hair dresser if I had had a pair of decent scissors and thought I could make myself look presentable, I would have taken them to my own hair long before I found myself sitting in her chair holding 7 inches of my hair! Here is a pic if you haven't seen it yet. :)

That's all for now...I have the rumblings of another post in my head that is way more serious and completely off topic, so I better start on that one before it's another two years til you see a new post. ;)

Labels: car, change, hair, happy, new job

Transitions

I, Paula Lopez, am writing a blog. I've always thought they were ridiculous and couldn't possibly imagine anyone caring enough about my life to want to read frequent updates. But here I am, joining the masses.

I guess it's not such a bad thing, but I've always felt people censor themselves and write with their audience in mind rather than the truth. But I will do my best to write freely and openly.

With that said, I'll get on to bigger and better things. :) So, I'm currently working as a substance abuse counselor and feel that I'm not really in the right field. I feel as though I'm a fish out of water. Degrees in Psychology and Criminal Justice are helpful but not really useful in this field. I would be more equipped if I had a degree in Counseling or Addictions. I'm hoping to get more into the Criminal Justice field or the Court System soon. I guess everything happens for a reason and I haven't found another job yet because it's not my time but...what the hell is the hold up?!

On a brighter note though, I have a lot more free time to do the things I love. Like READING. I have read about 10 books this summer and can't seem to get enough. :) I have a mini book club (yes, I'm a dork) with some girlfriends and we exchange books when we're done. For avid readers like us, this is just as good as a weekly trip to Barnes & Noble!

Anyway, I think I've written too much so I'll save some for later posts. ;)

As My World Turns......

Sunday, May 9, 2010