AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Background

Evaluating and managing dizziness and vertigo can be extremely difficult. The source of imbalance can range from easily treatable (eg, dehydration) to more ominous (eg, brain tumor). CNS problems need to be distinguished from circulation insufficiency, chemical and hormonal imbalances, and peripheral inner ear disorders. This distinction is often difficult. This article discusses peripheral inner ear disorders, specifically endolymphatic hydrops. Although it may be similar to articles on Ménière disease and syndrome, the focus will be the on pathophysiology of endolymphatic hydrops.

Endolymphatic hydrops by definition refers to increased hydraulic pressure within the inner ear's endolymphatic system. This pressure accumulation causes the following tetrad of symptoms: (1) fluctuating hearing loss (sometimes good or bad); (2) episodic vertigo (can be violent); (3) tinnitus or ringing in the ears (usually low-tone roaring); and (4) aural fullness (pressure, discomfort, fullness sensation in the ears).

Endolymphatic hydrops often is used synonymously with Ménière disease and Ménière syndrome, which are thought to result from increased pressure within the endolymphatic system.

Ménière disease is idiopathic, whereas Ménière syndrome is secondary to another disease process (eg, thyroid disease, inner ear inflammation due to syphilis). This distinction is analogous to that in Bell palsy. If the source of facial paralysis is known, the diagnosis is not Bell palsy. Similarly, if the cause of vertigo is known, the diagnosis cannot be Ménière disease. Ménière syndrome may be secondary to various processes that interfere with normal production or resorption of endolymph (eg, endocrine abnormalities, trauma, electrolyte imbalance, autoimmune dysfunction, medications, infections [especially parasitic], hyperlipidemia).

Pathophysiology

The endolymph and perilymph (ie, fluids that fill the chambers of the inner ear) are separated by thin membranes that house the neural apparatus of hearing and balance. Fluctuations in pressure stress these nerve-rich membranes, causing hearing disturbance, tinnitus, vertigo, imbalance, and a pressure sensation in the ear.

Attacks of hydrops probably are caused by an increase in endolymphatic pressure, which, in turn, causes a break in the membrane that separates the perilymph (potassium-poor extracellular fluid) and the endolymph (potassium-rich intracellular fluid). The resultant chemical mixture bathes the vestibular nerve receptors, leading to a depolarization blockade and transient loss of function. The sudden change in the rate of vestibular nerve firing creates an acute vestibular imbalance (ie, vertigo).

The physical distention caused by increased endolymphatic pressure also leads to a mechanical disturbance of the auditory and otolithic organs. Since the utricle and saccule are responsible for linear and translational motion detection (as opposed to angular and rotational acceleration), irritation of these organs may produce nonrotational vestibular symptoms.

The organ of Corti is disturbed mechanically. Distortion of the basilar membrane and the inner and outer hair cells may cause hearing loss and/or tinnitus. Since the apex of the cochlea is wound much tighter than the base, the apex is more sensitive to pressure changes than the base. This explains why hydrops preferentially affects low frequencies (at the apex) as opposed to high frequencies (at the relatively wider base). Symptoms improve after the membrane is repaired as sodium and potassium concentrations revert to normal.

Frequency

United States

Although probably underestimated, a prevalence of 1,000 cases per 100,000 population is a reasonable approximation. Familial predisposition may be a factor, since half of patients have a significant family history.

Mortality/Morbidity

Although the disease itself is not fatal, it can be associated with significant morbidity.

• Vertigo can cause accidents and falls, which can be devastating.
• Hearing loss often is progressive over time.
• Many patients can no longer work and are forced to claim disability.

Sex

The female-to-male ratio is 1.8:1.

Age

• The mean age among treatment groups in some studies ranged from 49-67 years.
• Ménière can be seen at almost all ages, but the typical onset begins at early to middle adulthood.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

History

The typical history involves episodic attacks of true whirling vertigo, which usually are preceded by a variable sense of ear pressure and fullness, decreased hearing, and a low-tone roaring tinnitus.

• The vertiginous attacks typically last minutes to hours, and often are associated with severe nausea and vomiting.
• After the acute attack, patients generally feel tired, unsteady, and nauseated for hours to days.
• The timing and frequency of attacks is variable. Some patients can regularly predict an attack while others note a completely random pattern. Attacks may be linked to dietary triggers, the menstrual cycle, or psychosocial stresses.
• Between episodes, some patients are completely symptom free. Many notice progressive deterioration of hearing and balance function with each successive attack.

Physical

Examination results vary, depending upon the phase of disease. During remission, physical examination findings may be completely normal, particularly if the patient is symptom free.

• During an acute attack, the patient has severe vertigo.
• Patients are often in significant distress. Many present to the physician's office clutching a bucket and towel with signs of recent vomiting.
• Patients are sometimes diaphoretic and pale.
• Vital signs may show elevated blood pressure, pulse, and respiration.
• Significant nystagmus may be present.
• Pneumo-otoscopy of the affected ear may elicit symptoms or cause nystagmus.
• The Romberg test generally shows significant instability and worsening when the eyes are closed.
• The Fukuda marching step test may show significant deviation (if the patient can stand with closed eyes).
• The Dix-Hallpike test result may be positive, indicating coexisting benign positional vertigo.
• Hearing usually is affected.
• The Weber tuning fork test usually lateralizes away from the affected ear.
• The Rinne test usually indicates that air conduction remains better than bone conduction.
• Complete neurologic evaluation is important. New-onset vertigo might be an early sign of stroke, migraine, or brainstem compression that may require emergent evaluation and care.

Causes

• Several disorders may cause increased endolymph pressure, including metabolic disturbances, hormonal balance, and various infections.
• Autoimmune diseases, such as lupus and rheumatoid arthritis, may cause an inflammatory response within the labyrinth.
• Allergy also has been implicated in many patients with "difficult to treat" Ménière.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Other Problems to be Considered

Neurosyphilis
Viral infections
Trauma
Congenital anomalies
Microvascular compression syndromes
Rheumatoid arthritis
Susac syndrome
Cogan syndrome
Inner ear inflammation
Otosclerosis
Perilymphatic fistula
Electrolyte imbalance
Hyperlipidemia
Diabetes
Vertigo
Vestibular neuronitis
Acoustic neuroma

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• Blood tests: Several are used to exclude obvious metabolic disturbances, infections, and/or hormonal imbalances.
• • Thyrotropin, T4, T3
  • Serum glucose
  • Sedimentation rate (ESR)
  • Antinuclear antibody
• Complete blood cell (CBC) count
• Electrolytes
• Venereal Disease Research Laboratory test (VDRL) and fluorescent treponemal antibody–absorbed (FTA-ABS) for neurosyphilis
• Allergy testing for allergy-mediated Ménière syndrome
• Lyme disease testing
• Urinalysis for proteinuria, hematuria, or other indicators of otorenal syndrome

Imaging Studies

• Magnetic resonance imaging
• • Brain scan should be done to rule out abnormal anatomy or mass lesions. Specifically, acoustic neuromas or other cerebellopontine angle lesions are sought. Other lesions, such as multiple sclerosis or Arnold-Chiari malformations, also can be ruled out.
  • Note that mass lesions rarely are found but are important to exclude.
• CT scans reveal dehiscent superior semicircular canals and/or widened cochlear and vestibular aqueducts.

Other Tests

• Audiometry is particularly helpful to document present hearing acuity and to detect future change.
• • The patient may not notice a loss at specific frequencies. Low-frequency or mixed low- and high-frequency insufficiency may be observed.
  • Typically, the lower frequencies are affected more severely. This is due to preferential sensitivity of the apex to the hydrops.
  • Multiple hearing tests, which document fluctuating hearing loss, are helpful in diagnosing Ménière.
• Transtympanic electrocochleography (ECOG) specifically detects distortion of the neural membranes of the inner ear.
• • This is presumably due to perilymph pressure fluctuations and can show evidence of cochlear involvement.
  • ECOG measures the ratio of the summating potential (probably from the movement of the basilar membrane) and the nerve action potential in response to auditory stimuli. Hydrops is suggested when this ratio is greater than 35%.
  • This is most accurate when Ménière is active.
• Electronystagmography (ENG) is a test of the inner ear function (particularly the semicircular canals).
• • Administer the test when the patient has an empty stomach and after discontinuing meclizine (Antivert), antihistamines, and sedatives for 2 weeks. These drugs may alter test results.
  • The patient may feel dizzy or nauseated. The test determines inner ear responsiveness to movement and caloric stimulation.
  • It tests central and peripheral function and can help localize the site of lesion.
  • Typically, endolymphatic hydrops causes a reduced vestibular response in the affected ear, although response may be increased secondary to an irritative lesion.
  • The direction of the spontaneous nystagmus during or after an attack of Ménière is not a reliable indicator of the site of the lesion. An irritative phase may occur during the attack (fast phases directed toward involved ear) followed by a paretic phase (fast phases directed toward opposite ear).

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Medical Care

Medical therapy can be directed towards treating the actual symptoms of the acute attack or directed towards prophylactic prevention of the attacks.

• If endolymphatic hydrops is attributable to a given disease process (and thus called Ménière syndrome), the first-line management is diagnosis and treatment of the primary disease (eg, thyroid disease).
• Vestibulosuppressants (eg, meclizine, droperidol, prochlorperazine [Compazine], diazepam [Valium], lorazepam [Ativan], alprazolam [Xanax]) decrease symptoms, but generally only mask the vertigo by decreasing the brain's response to vestibular input.
• Diuretics or diureticlike medications (eg, hydrochlorothiazide, hydrochlorothiazide/triamterene [Dyazide], acetazolamide [Diamox], methazolamide [Neptazane]) actually decrease the fluid pressure load in the inner ear. These medications help prevent attacks but do not help once an acute attack has started.
• Anti-inflammatory properties of steroids are helpful in endolymphatic hydrops. Some researchers believe that steroids reduce endolymphatic pressure by reducing edema. Steroids actually can reverse symptoms of vertigo, tinnitus, and hearing loss.
• Aminoglycosides are a class of antibiotics that were discovered serendipitously to be preferentially toxic to the vestibular end organ.
• The histamine agonists are used in countries outside the United States must be mentioned. Medications such as betahistine (Serc) are widely used in Europe and South America. Although its mechanism of action is somewhat controversial, many have reported success with its use in mitigating symptoms of Ménière disease. Unfortunately, since betahistine (Serc) is not approved by the US Food and Drug Administration, it is not discussed much in the United States.
• • Destruction of the vestibular end organ renders the brain insensitive to the fluctuations in the inner ear pressure during an acute Ménière attack.
  • If given systemically, aminoglycosides affect both ears.
  • Although these drugs can be used to treat extremely severe bilateral Ménière disease, they leave the patient with little or no balance function. The resulting Dandy syndrome, a complete loss of inner ear function, can be debilitating.
  • Other routes of administration, in particular transtympanic injection, are discussed in Surgical Care.
• During the quiescent phase, medical treatment of Ménière disease is tailored to each patient. Lifestyle and dietary changes are usually the first step. Avoiding trigger substances (eg, salt, chocolate, caffeine) alone may be sufficient. Smoking cessation also is recommended.
• If medications are required, a 3-month trial of a diuretic (eg, hydrochlorothiazide/triamterene) and dietary management are prescribed.
• • Typically, vestibulosuppressants and antinausea medications (eg, meclizine, prochlorperazine) are prescribed for prn use.
  • Note that frequent and long-term use of these medications is not recommended. Long-term use of vestibulosuppressants can lead to bad vestibular compensation skills and result in poor balance function. Sedative effects can affect patient productivity. Furthermore, long-term tachyphylaxis may result.
• In an acutely vertiginous patient, management is directed toward vertigo control.
• • Intravenous (IV) or intramuscular (IM) diazepam provides excellent vestibular suppression and antinausea effects.
  • Steroids can be given for anti-inflammatory effects in the inner ear.
  • IV fluid support can help prevent dehydration and replaces electrolytes.

Surgical Care

Surgical therapy for Ménière disease is reserved for medical treatment failures and is otherwise controversial. Historically, several surgical procedures have been invented, tested, and discarded. Surgical procedures are divided into 2 major classifications as follows:

• Destructive surgical procedures
• • Rationale to control vertigo: Endolymphatic hydrops causes fluid pressure accumulation within the inner ear, which causes temporary malfunction and misfiring of the vestibular nerve. These abnormal signals cause vertigo. Destruction of the inner ear and/or the vestibular nerve prevents these abnormal signals from reaching the brain. As long as the opposite inner ear and vestibular apparatus function normally, the brain eventually will compensate for the loss of one labyrinth over the following weeks to months.
  • Problems with destructive procedures: Destruction of one inner ear depends on the adequate function of the opposite ear. Unfortunately, Ménière disease can be bilateral (7-50%), in which case this method is contraindicated. Since balance and hearing are closely intertwined within the labyrinth, destruction of the balance portion carries a high risk of hearing loss. Note that destructive procedures are irreversible and reserved for severe cases.
• Nondestructive surgical procedures
• • These are directed toward improving the state of the inner ear. They are less invasive than destructive procedures and do not preclude the use of other treatment modalities. Discussion here is limited to the 4 most generally accepted management options: (1) endolymphatic sac decompression or shunt, (2) vestibular nerve section, (3) labyrinthectomy, and (4) transtympanic medication perfusion.
  • Endolymphatic sac decompression and/or shunt
    • In theory, the endolymphatic sac procedure decreases endolymph pressure accumulation by removing the petrous bone, which encases the endolymph reservoir. This procedure allows the reservoir sac to expand more freely, thus dissipating pressure. A drain or valve from the endolymphatic space to either the mastoid or subarachnoid space can be inserted as another means of further reducing pressure.
    • Success rates (in terms of controlling vertigo and stabilizing hearing acuity) with this procedure are reported at 60-80%. These success rates do not seem to differ significantly from those of endolymphatic sac decompression coupled with shunt procedures. Morbidity and mortality rates of endolymphatic sac decompression are relatively low. The risk of hearing loss and facial nerve damage is minimal in experienced hands. Severe postoperative pain is unusual; in most cases the recovery period is typically short and uneventful.
    • The endolymphatic sac procedure is one of the most controversial issues in neurootology. Citing the famous Danish study, critics argue that endolymphatic surgery is no more effective than sham surgery and that any benefit is due to placebo effect. Proponents argue that patients indeed improve and, compared to destructive procedures, the endolymphatic sac procedures have low risk and morbidity rate. These procedures may provide relief in patients who have not responded to medical therapy.
    • Exposing the endolymphatic sac is essentially an extended mastoidectomy. Special care is taken to skeletonize the sigmoid sinus, posterior fossa dura, and posterior semicircular canal. The thin, egg-shelled bone is removed from the posterior fossa dura and sigmoid sinus. The endolymphatic sac is distinguished from dura by color and texture differences. The sac is thicker and whiter than the surrounding tissue. The location of the sac can vary, but it is generally immediately posterior or posterior inferior to the posterior semicircular canal. In endolymphatic sac decompression, the procedure is terminated after all of the bone overlying the sac is removed. The shunt procedures involve incising the lateral leaf of the sac and inserting a drainage tube into the internal lumen of the endolymphatic duct. As already mentioned, the shunt can drain into either the subarachnoid space or the mastoid space.
  • Vestibular nerve section
    • For patients with useful hearing in the affected ear, sectioning the diseased vestibular nerve can be the ultimate solution. Although the hearing and balance functions are housed in one common chamber within the inner ear, their neural connections to the brain separate into distinct nerve bundles as they course through the internal auditory canal. This anatomical separation allows balance function to be isolated and ablated without affecting hearing function. Because this surgery opens the internal auditory canal, it is similar to the approaches for an acoustic neuroma. Vestibular nerve sections typically are done through either a retrosigmoid or middle fossa approach. The translabyrinthine approach does not spare hearing. It is used only for added insurance when labyrinthectomy is intended.
    • Vestibular nerve section has the advantage of a high rate of vertigo control (95-98%) with hearing preservation in the operated ear (95% successful). Risks of this procedure, although rare, are similar to those of craniotomy and acoustic neuroma surgery and include the following: facial nerve damage, hearing loss, exacerbation of tinnitus and dizziness, cerebrospinal fluid leakage, headaches, hemorrhage, and infection (eg, meningitis). Postoperatively, patients generally require 3-5 days of inpatient care. Accommodation to the surgical loss of one vestibular apparatus usually takes weeks to months. Vestibular rehabilitation during this time period is often helpful.
    • Retrosigmoid approach: Most agree that the retrosigmoid (accomplished through a small craniotomy, posterior to the sigmoid sinus) is technically less difficult than the middle fossa approach. Exposure of the cerebellopontine angle allows visualization of the eighth cranial nerve. Proper identification of the vestibular nerve is mandatory to avoid severing the facial nerve and cochlear nerve. Proper anatomical relationships must be confirmed. Because the nerve bundle rotates as it exits the internal auditory canal, the vestibular nerve moves from its lateral position to a more superior location. The vestibular nerves are closest to the tentorium. Facial nerve and cochlear nerve monitoring via intraoperative audiometric brainstem responses is essential.
    • Middle fossa approach: This approach for vestibular nerve section is more technically complex than the retrosigmoid approach. The procedure creates a 5 cm by 5 cm middle fossa craniotomy just superior to the temporal line above the external ear canal. The middle fossa dura is retracted superiorly to expose the bone. After proper anatomical landmarks are identified, the search for the internal auditory canal begins. Once the internal auditory canal is found and opened, the vestibular nerve is sectioned as laterally as possible. Fat is packed into the internal auditory canal and held in position by the temporal lobe dura. Finally, the craniotomy is closed.
    • Advantage of the middle fossa approach is a slightly more complete ablation of vestibular function. Because the vestibular fibers are cut immediately as they exit the vestibular end organ, the chance of stray vestibular fibers crossing over to travel along the facial and cochlear nerves is minimal. The retrosigmoid approach sections the vestibular nerve more medially, potentially after stray vestibular fibers have already crossed. Although unusual, failure of the retrosigmoid approach may be due to these crossed fibers.
    • Disadvantages of the middle fossa approach include the difficulty in finding the internal canal and the limited exposure within the canal because of the facial nerve's position. Cutting the vestibular nerve without exerting pressure on the cochlear and facial nerves is difficult, since the vestibular bundle lies deep within the canal. The risk of damaging the cochlear artery, with resulting hearing loss, is significant.
  • Labyrinthectomy
    • This management option for Ménière disease has the advantage of a high cure rate (>95%) and is useful in the patient whose hearing on the diseased side has been destroyed already by Ménière disease. Labyrinthectomy involves ablation of the diseased inner ear organs. This procedure is less complex than vestibular nerve section because labyrinthectomy does not require entry into the cranial cavity. Labyrinthectomy is less invasive than vestibular nerve section.
    • This procedure carries less danger of cerebrospinal fluid leak and meningitis since craniotomy is not required. Like those who undergo vestibular nerve section, patients require a few days of inpatient care. Accommodation to the surgical loss of one vestibular apparatus usually takes weeks or months. Vestibular rehabilitation during this time period is also helpful.
    • The transcanal approach is done through the external ear canal. A tympanomeatal flap is first elevated. Next, a right angle pick is inserted through the oval window and maneuvered to disrupt and scramble the nerve tissues of the labyrinth. A drill can be used to connect the round window and oval window to obtain better exposure to the neuroepithelium.
    • The basic mastoidectomy approach involves extension of the mastoidectomy by drilling through the semicircular canals, allowing a more complete ablation of the labyrinthine neuroepithelium than the transcanal approach.
  • Transtympanic perfusion of medication
    • This relatively new modality of treatment was popularized by Dr. John Shea in 1995. The procedure is still evolving and, although variations have been devised, the concept remains the same. Medications for Ménière disease are applied through a myringotomy within the middle ear cavity, where they presumably are absorbed through the round window membrane into the inner ear. Transtympanic perfusion is a relatively low-risk, simple procedure that applies a high concentration of medicine with minimal systemic effects. It is similar to the placement of tympanostomy tubes, which can be done in the office or in an outpatient setting.
    • Recent innovations such as the round window microcatheter have been designed to direct the flow of medication directly to the round window niche. This method theoretically reduces dosing inconsistencies due to wastage down the eustachian tube. It also allows for slow, continuous micropump infusion.
    • If steroids are administered with this transtympanic technique, the surgery is classified as nondestructive. Transtympanic steroid application is useful, particularly when patients have poor tolerance for the systemic side effects of steroids. A higher concentration can be obtained using this approach. Success rates seem favorable, although long-term studies are unavailable.
    • If aminoglycosides are used, the surgery is classified as destructive. When given transtympanically, aminoglycosides can concentrate their effects in the affected ear.
    • Since streptomycin is difficult to obtain in the United States owing to Food and Drug Administration (FDA) restrictions, gentamicin is used more widely. Early studies show about 90% efficacy. Some authors report significant worsening of hearing in 5-15% of patients.
  • The Meniett device
    • One recent innovation in the treatment of Ménière disease is the Meniett device. Its use is not precisely a medical treatment, and the device itself does not require surgical installation. It does, however, require insertion of a tympanostomy tube so that the device can work; therefore, its use may qualify as a surgical treatment.
    • The Meniett device delivers pulses of pressure to the inner ear via the tympanostomy tube.
    • Although exactly why this works remains unknown, some patients have symptomatic relief when the device is used on a daily basis. Because it is new, long-term results have not been fully evaluated.

Consultations

Differential diagnosis is vast, so consider obtaining consultations from specialists.

• Otolaryngologist
• Neurologist
• Cardiologist
• Endocrinologist
• Internist
• Physical medicine (especially in the postoperative period) specialist

Diet

• Dietary management is appropriate in patients not severely affected; patients avoid substances that may trigger or exacerbate fluid pressure buildup in the inner ear.
• Similar to managing systemic hypertension, the goal for Ménière disease is to reduce the total body fluid volume. This, in turn, may reduce the inner ear fluid volume.
• • Since sodium seems to play a major role in fluid retention within the inner ear, avoiding salt (eg, pizza, preserved foods, smoked fish) is paramount.
  • Consult with a nutritionist to establish a rigid salt-restricted diet (1.5 g sodium per day).
  • Avoiding other trigger substances (eg, caffeine, nicotine, alcohol, high-carbohydrate substances, high-cholesterol/triglyceride foods) also can help.
  • Note that many preserved and smoked foods contain sodium nitrite, which can contribute to high sodium content.

Activity

• Endolymphatic hydrops does not preclude regular activity. Exercise is recommended in moderation.
• Because of the unpredictable nature of the disease, balance-intensive, dangerous tasks (eg, especially climbing ladders) should be avoided.

MEDICATION

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

The goals of pharmacotherapy are to reduce morbidity and prevent complications. Medication is for both symptomatic and prophylactic use.

Drug Category: Vestibulosuppressants

These agents decrease symptoms but generally only mask the vertigo. They dull the brain's response to the inner ear's signals. Examples include meclizine, dimenhydrinate, droperidol, perchlorperazine, diazepam, lorazepam, alprazolam, and scopolamine.

Drug Category: Benzodiazepines

These agents act as antiemetics and vestibulosuppressants by binding to specific receptor sites, which apparently potentiates the effects of GABA and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters.

Drug Category: Corticosteroids

The anti-inflammatory properties of steroids are helpful in treatment of endolymphatic hydrops, probably by reducing endolymphatic pressure; steroids actually can reverse the vertigo, tinnitus, and hearing loss.

Drug Category: Diuretics

Diuretics or diuretic-like medications actually can decrease fluid pressure load in the inner ear. These medications help prevent attacks but are ineffective once an attack is triggered. Examples include hydrochlorothiazide, hydrochlorothiazide/triamterene, acetazolamide, and methazolamide.

Drug Category: Anti-emetic agents

These are useful in the treatment of nausea caused by vertigo.

FOLLOW-UP

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Further Inpatient Care

• Aside from acute control of vertigo and associated effects (eg, dehydration from protracted vomiting), inpatient care is generally unnecessary.

Further Outpatient Care

• Vestibular rehabilitation can be helpful in teaching patients to cope with vertigo and imbalance.

Deterrence/Prevention

• Dietary control and avoiding trigger substances may prevent acute episodes.

Complications

• See Pathophysiology and Causes.

Prognosis

• Prognosis is variable, since the disease pattern of exacerbation and remission makes evaluation of treatment and prognosis difficult to predict.
• • In general, Ménière symptoms tend to stabilize spontaneously with time. With regard to vertigo, about half of patients stabilize over several years.
  • Patients tend to "burn out" over time and with residual poor balance and hearing.
• Ménière disease can be classified into several stages of progression. Early stages involve cochlear hydrops, which proceeds to affect the vestibular system.
• Ménière disease is most bothersome during these early stages.
• • As patients progress to later stages, the hydrops fills the vestibule so completely that no further room is available for pressure fluctuation and the vertigo spells disappear.
  • The acute attacks are replaced by constant imbalance and progressive hearing loss.

Patient Education

• Proper education in terms of dietary control and avoidance techniques is helpful.
• Vestibular rehabilitation can be helpful in teaching patients to cope with the vertigo and imbalance.
• For excellent patient education resources, visit eMedicine's Brain and Nervous System Center and Ear, Nose, and Throat Center. Also, see eMedicine's patient education articles Dizziness, Ménière Disease, and Tinnitus.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

• Bretlau P, Thomsen J, Tos M, Johnsen NJ. Placebo effect in surgery for Meniere''s disease: nine-year follow-up. Am J Otol. Jul 1989;10(4):259-61. [Medline].
• Densert B, Sass K. Control of symptoms in patients with Meniere's disease using middle ear pressure applications: two years follow-up. Acta Otolaryngol. Jul 2001;121(5):616-21. [Medline].
• Ernst A, Basta D, Seidl RO, et al. Management of posttraumatic vertigo. Otolaryngol Head Neck Surg. Apr 2005;132(4):554-8. [Medline].
• Glasscock ME 3rd, Jackson CG, Poe DS, Johnson GD. What I think of sac surgery in 1989. Am J Otol. May 1989;10(3):230-3. [Medline].
• Green JD Jr, Blum DJ, Harner SG. Longitudinal followup of patients with Meniere''s disease. Otolaryngol Head Neck Surg. Jun 1991;104(6):783-8. [Medline].
• Monsell EM, Wiet RJ. Endolymphatic sac surgery: methods of study and results. Am J Otol. Sep 1988;9(5):396-402. [Medline].
• Pyykko I, Ishizaki H, Kaasinen S, Aalto H. Intratympanic gentamicin in bilateral Meniere''s disease. Otolaryngol Head Neck Surg. Feb 1994;110(2):162-7. [Medline].
• Semaan MT, Alagramam KN, Megerian CA. The basic science of Meniere's disease and endolymphatic hydrops. Curr Opin Otolaryngol Head Neck Surg. Oct 2005;13(5):301-7. [Medline].
• Shea JJ Jr. Classification of Meniere''s disease. Am J Otol. May 1993;14(3):224-9. [Medline].
• Shea JJ Jr, Ge X. Streptomycin perfusion of the labyrinth through the round window plus intravenous streptomycin. Otolaryngol Clin North Am. Apr 1994;27(2):317-24. [Medline].
• Silverstein H, Smouha E, Jones R. Natural history vs. surgery for Meniere''s disease. Otolaryngol Head Neck Surg. Jan 1989;100(1):6-16. [Medline].
• Silverstein H, Lewis WB, Jackson LE, et al. Changing trends in the surgical treatment of Meniere's disease: results of a 10-year survey. Ear Nose Throat J. Mar 2003;82(3):185-7, 191-4. [Medline].

Article Last Updated: Jan 16, 2007