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There are many causes of dizziness. The term "dizziness" should be substituted for more descriptive words to describe your symptoms. Words such as vertigo, which indicates a sensation of movement or spinning, as well as lightheadedness or faintness are more helpful to your doctor when trying to diagnose the specific cause of your "dizziness".

There are many causes of dizziness and a few of the structures that may be involved are the eyes, the inner ear, the brain and/or the neck. Disorders of the neck will generally give you ”odd“ feelings but rarely true vertigo.

The vestibular apparatus is the name of the structure in your inner ear responsible for balance and thus physiotherapy designed to restore balance and a sense of stability is termed Vestibular Rehabilitation Therapy (VRT). We have included specific information about many vestibular and non-vestibular causes of dizzines for you to read. Most of this information was extracted from the Vestibular Disorders website.

Dizziness Information

play button Benign Paroxysmal Positional Vertigo Videos

The majority of people presenting with symptoms of vertigo, a sensation of movement or spinning, will be diagnosed as having Benign Paroxysmal Positional Vertigo or BPPV.

This is further classified clinically to indicate the canal of involvement and whether or not the displaced stones are free floating or stuck on another structure.

We have included short film clips that show the doctor performing the diagnostic and repositioning maneuvres as well as the patient undergoing the maneuvres wearing special goggles. These goggles record the characteristic, automatic eye movements that occur when structures in the inner ear are stimulated. Most importantly, there is an animated illustration included that depicts what is happening inside the inner ear canals so that you can see exactly what the repositioning maneuvres are attempting to accomplish.

The film clips were produced by Bernard Cohen ENT department, hôpital Saint-Antoine, Paris. BPPV was first described at the beginning of the twentieth century by Barany. It was not until 1952 that Dix and Hallpike described the diagnostic manoeuvre.

These videos are encoded to run with an embeded Adobe Flash player. If you are experiencing difficulties watching the videos, try installing the latest version.

In order to view these videos fullscreen, please click this button on the player:

BPPV Introduction

Posterior Canal BPPV

Lateral Canal BPPV

Anterior Canal BPPV

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Vestibular Rehabilitation Therapy

Why is therapy needed?

If the brain cannot rely on the information it receives from the vestibular system, a person's ability to maintain posture and coordinate balance can become overly dependent on vision or on the information received from the muscles and joints (proprioception).

This can lead to developing new patterns of movement to compensate for the change and to avoid head movements that are apt to create symptoms of dizziness and nausea. For example, a person might adopt an exaggerated hip sway as a method of balancing, might swivel the entire body rather than just the head in turning to look at something, or might always look down at the floor to avoid what appears as a confusing swirl of activity.

Unfortunately, these types of adaptation can result in headache, neckache, muscle stiffness, general fatigue, and a decrease in the ability to retrain the brain to adjust to the vestibular problem, hence making the symptoms much worse.

The goal of VRT is to retrain the brain to recognize and process signals from the vestibular system in coordination with information from vision and proprioception. This often involves desensitizing the balance system to movements that provoke symptoms.

What happens during vestibular therapy?

A qualified therapist will first perform a thorough evaluation. This includes observing posture, balance, movement, and compensatory strategies. Using the result of this evaluation, the therapist will develop an individualized treatment plan that will include exercises to be performed both in the therapy department and at home and that combine specific head and body movements with eye exercises. Many times, treatment may also include increasing activities and exercise in order to strengthen muscles and increase tolerance for certain stimuli.

Some of the exercise and activities may at first cause an increase in symptoms, as the body and brain attempt to sort out the new pattern of movements. But with time and consistent work, the coordination signals from the eyes, proprioception, and vestibular system will occur.

How does therapy help?

In most cases, balance improves if the exercises are correctly and faithfully performed. Muscle tension, headaches, and fatigue will diminish, and symptoms of dizziness, vertigo, and nausea will decrease or disappear. Many times, vestibular VRT is so successful that no other treatment is required.

Occassionally surgery will be required to correct an inner ear problem. Often, therapists provide further therapy after a person has recovered from the surgery.

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Why do I feel dizzy?

To understand why we feel dizzy, we first need to describe how the body senses movement. There are three systems or inputs that feed information to the brain regarding your head position in space:

  1. The first is visual input. Our eyes observe our surroundings and tell the brain if we are moving or stationary.
  2. The second is input from the body sensors that exist in joints, ligaments and muscles. These sensors allow us to feel where our feet are in space. Closing your eyes and trying to maintain your balance on one leg clearly demonstrates this.
  3. The final input to the brain, consisting of acceleration/deceleration data, is from a very small structure in the inner ear known as the vestibular apparatus.

The brain takes all the information from these three inputs and compares them against one another for consistency. If they are all telling the brain the same thing about our movement then we feel “normal” and not “dizzy”.

One condition causing “dizziness” is termed Benign Paroxysmal Positional Vertigo (BPPV) and is described below.

The vestibular apparatus of the inner ear consists of two central organs and three surrounding half circle tubes or canals, which are filled with liquid. There are jelly-like structures in the central organs that have rock-type crystals on top of them, i.e. like pebbles on a jelly mold. Sometimes these crystals/pebbles suddenly fall off the jelly mold and roll into one of the surrounding semi-circular tubes. These crystals will then roll around inside these half circle tubes moving the fluid and sending the brain incorrect information about how we’re moving in space. People may even experience a feeling of their eyes moving involuntarily due to the connection between the inner ear and the eyeball muscles. This connection can be stimulated by the out-of-place crystals in the semi-circular tubes, which, in turn, stimulates the eyeball muscles causing the eyes to move. This movement is termed nystagmus.

The goal of therapy for BPPV is to put the out-of-place crystals back where they belong by a series of careful head maneuvers. The maneuvers that are performed are determined by which semi-circular canal has been affected. We can tell which canal is affected by looking at the automatic eye movements that are seen while you wear special infrared goggles. The success of the movements can be instantaneous. To determine if you are a candidate for this type of therapy call us.

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Causes of Dizziness, Vertigo, and Imbalance

A large percentage of the adult population reports episodes of dizziness or vertigo to a physician during their lifetime. Many of these cases involve vestibular (inner ear) disorders. Other cases of dizziness are due to problems unrelated to the inner ear, such as cardiovascular, neurological, or psychological disorders.

  • Dizziness caused by vestibular disorders
  • Dizziness from non-vestibular causes

Dizziness Caused by Vestibular Disorders

The vestibular organs of the inner ear provide the brain with information about changes in head movement. If the vestibular system is not functioning properly, dizziness, vertigo, imbalance, spatial disorientation, and other symptoms can result.

Vestibular-system distress can be caused by a variety of influences, including viral infections of the labyrinth (labyrinthitis) or the vestibular nerve (vestibular neuritis). Bacterial infection of either the middle ear (otitis media) or the brain coverings (meningitis) may spread to the inner ear. Allergies can cause changes in the inner ear fluids or middle ear pressure because of swelling of the Eustachian tube and production of fluid in the middle ear.

Head trauma is a common cause of inner ear damage in people under age 50. A blow to the head or a "whiplash" injury can result in, for example, perilymph fistula or benign paroxysmal positional vertigo (BPPV). Vestibular-system dysfunction may appear immediately following head trauma or after a delay of days, weeks, or months.

Vestibular disorders can also occur from exposure to ototoxins (drugs or chemicals that are harmful to the inner ear or the vestibulo-cochlear nerve). Degeneration of the hair cells in the inner ear is also thought to occur with aging and can result in dizziness and vertigo as well as hearing loss. A benign tumor known as an acoustic neuroma can grow on the vestibulo-cochlear nerve. In many cases of vestibular disorders, including Meniere's disease and other forms of endolymphatic hydrops, the underlying or original cause cannot be determined.

Other conditions that may affect vestibular function include migraine, mal de debarquement (a sensation of rocking that persists after a cruise or other travel), autoimmune inner ear disease, cervical (neck) problems, vascular compression of the vestibular nerve, superior canal dehiscence, cholesteatoma, enlarged vestibular aqueduct, and others.

Dizziness from Non-Vestibular Causes

Dizziness is the second most common complaint heard in doctors’ offices (after lower back pain). Dizziness has many causes other than inner ear dysfunction.

Visual disturbances can result in lightheadedness or dizziness. Some people feel dizzy while adjusting to bifocals or a new eyeglass prescription, or from reduced vision due to cataracts.

Hyperventilation can cause temporary dizziness. During rapid breathing, more carbon dioxide than normal is expelled and the level of carbon dioxide in the blood falls, which in turn affects the function of brain cells.

Decreased blood flow to the brain or brain stem can cause dizziness, because insufficient oxygen is reaching the cells. Conditions that can reduce blood flow to the brain include orthostatic hypotension (low blood pressure upon suddenly rising from a lying or sitting position), dehydration, vasovagal syndrome (a nervous-system response that causes sudden loss of muscle tone in peripheral blood vessels), arteriosclerosis (hardening or narrowing of blood vessels), and osteoarthritis (a joint disease that can narrow the openings in the neck vertebrae through which blood vessels flow).

Nervous-system disorders such as peripheral neuropathies (diminished nerve function in the legs or feet) can cause unsteadiness. A tumor may affect the brain stem, the cerebellum (the coordination center of the brain), or the part of the cerebral cortex that controls voluntary muscle movements.

Even stress, tension, or fatigue may cause dizziness. Under these conditions, the brain stem functions less efficiently, resulting in some loss of automatic reflex control of balance. This leads to elevated levels of activity for the cerebral cortex, as conscious energy is used to help maintain balance by controlling voluntary muscle movements.Lightheadedness and unsteadiness can result.

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Vestibulo-Ocular Reflex

The vestibulo-ocular reflex is a reflex that allows us to maintain a stable gaze in which our eye is fixated on an object when we are moving our head. To illustrate we'll get you to look at the words on this screen and while reading turn your head to the right all the while maintaining focus on these words. What just happened? Did your eyes move? If they moved with your head then you'd now be gazing to the right in the direction your head turned. In fact your eyes moved in exactly the opposite direction at exactly the same speed as your head. So, if your head moved right at 20 degrees/sec then your eyeballs moved left at 20 degrees/second. This amazing ability of the eyes to simultaneously perform the opposite movement to that of the head is driven by the vestibulo-ocular reflex. This reflex is calibrated in the brain so that the speed of the head equals speed of the eyes but in opposite directions. This calibration ratio must be 1 for if it were less or more the eyes would move more slowly or quickly than the head and you wouldn't be able to keep the object you'd be looking at in focus.

Unfortunately, if an individual is afflicted with vestibular abnormalities that feed abnormal information to the brain over long periods of time, this calibration ratio can indeed change so it is no longer 1. An example of someone whose vestibulo-ocular reflex may have changed would be someone with Meniere's disease whose had repeated, prolonged bouts over a long time period. Symptoms of this type of reflex abnormality would include feelings of "dizziness" when driving on the highway looking at fast moving traffic, walking in a mall or generally being in crowds. Vestibular rehabilitation therapy can address this altered ratio by instrucing the person in gaze stabilization exercises called adaptation exercises.

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Specific Vestibular Disorders

Benign Paroxysmal Postitional Vertigo (BPPV)

Benign paroxysmal positional vertigo (BPPV) is a disorder that causes vertigo, dizziness, and other symptoms due to debris that has collected within a part of the inner ear. This debris, called otoconia, is made up of small crystals of calcium carbonate (sometimes referred to colloquially as “ear rocks”). With head movement, the displaced otoconia shift, sending false signals to the brain.

Symptoms of BPPV are almost always precipitated by a change in head position. Getting out of bed and rolling over in bed are two common "problem" motions. Some people feel dizzy and unsteady when they tip their heads back to look up. An intermittent pattern of these symptoms is usual.

About 20% of all dizziness is due to BPPV. The most common cause of BPPV in people under age 50 is head injury. About 50% of dizziness in older people is due to BPPV. In half of all cases, BPPV is idiopathic, which means that it occurs for no known reason. BPPV is also associated with migraine.

Diagnostic tests for BPPV include tests that look for the characteristic nystagmus (jumping of the eyes), such as the Dix-Hallpike test and electronystagmography (ENG).

Particle-repositioning maneuvers, including the Epley maneuvre and the Semont-liberatory maneuver, are very effective in treating BPPV and can be performed in the doctor’s office in about 15 minutes. The goal of these maneuvers is to move the detached otoconia out of one of the semicircular canals. Treatment may also include individualized vestibular physical therapy exercises designed to help “retrain the brain.” The Brandt-Daroff habituation exercises are sometimes recommended and can be done at home. Canal-plugging surgery may be another option.

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Meniere’s Disease

Meniere‘s disease is a vestibular disorder that produces a recurring set of symptoms as a result of abnormally large amounts of a fluid called endolymph collecting in the inner ear.

The prevalence of Meniere's disease is difficult to assess. One population study found that 15.3 per 100,000 individuals develop Meniere's disease annually. Of these, one-third eventually develop the disease in the second ear as well.

The exact cause of Meniere's disease is not known. Theories include circulation problems, viral infection, allergies, an autoimmune reaction, migraine, and the possibility of a genetic connection. Experts also aren't sure what generates the symptoms of an acute attack. Some people with Meniere's disease find that certain triggers can set off attacks, including stress, overwork, fatigue, emotional distress, additional illnesses, pressure changes, certain foods, and too much salt in the diet.

Attacks can last from 20 minutes to 24 hours. They can occur many times per week; or they can be separated by weeks, months, and even years. The unpredictable nature of this disease makes it difficult to tell how it will affect a person's future. Symptoms can disappear one day and never return, or they might become so severe that they are disabling.


During an attack of early-stage Meniere's disease, the main symptoms are spontaneous, violent vertigo, fluctuating hearing loss, ear fullness, and/or tinnitus. Following the attack, a period of extreme fatigue or exhaustion often occurs, prompting the need for hours of sleep. The periods between attacks are symptom-free for some people and symptomatic for others.

Late-stage Meniere’s disease refers to a set of symptoms rather than a point in time. Hearing loss is more significant and is less likely to fluctuate. Tinnitus and/or aural fullness may be stronger and more constant. Attacks of vertigo may be replaced by more constant struggles with vision and balance, including difficulty walking in the dark and occasional sudden loss of balance. Sometimes, drop attacks of vestibular origin (Tumarkin's otolithic crisis) occur in this stage of Meniere's disease.


In the United States, the most conservative long-term treatment for Meniere’s disease (aimed at reducing the severity and number of attacks) involves adhering to a reduced-sodium diet and using diuretics, or "water pills." The goal of this treatment is to reduce inner ear fluid pressure. Some physicians, more commonly outside of the United States, also weigh the potential efficacy of using betahistine HCl (Serc) as a vestibular suppressant for Meniere’s disease.

Medications that are used during an attack to reduce the vertigo, nausea, and vomiting include diazepam (Valium), promethazine (Phenergan), dimenhydrinate (Dramamine Original Formula), and meclizine hydrochloride (Antivert, or Dramamine Less Drowsy Formula). Vestibular rehabilitation therapy is sometimes used to help with the imbalance that can plague people between attacks. Its goal is to help retrain the ability of the body and brain to process balance information.

Another recently introduced, conservative treatment approach employs a device to deliver a series of low-pressure air pulses designed to displace inner ear fluids. The use of this device is approved for general use by the U.S. Food and Drug Administration (FDA) and is currently undergoing clinical trials in the United States.

For the 20-40% of people who do not respond to medication or diet, a physician may recommend a chemical labyrinthectomy, which destroys vestibular tissue with injections into the ear of an aminoglycoside antibiotic (gentamicin). Another less conservative treatment is surgery to relieve the pressure on the inner ear (although this is not as widely used now as it was in the past) or to destroy either the inner ear or the vestibular nerve, so that balance information is not transmitted to the brain.

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Secondary Endolymphatic Hydrops

Endolymphatic hydrops may be either primary or secondary. Primary idiopathic endolymphatic hydrops known as Meniere's disease occurs for no known reason. Secondary endolymphatic hydrops appears to occur in response to an event or underlying condition. For example, it can follow head trauma or ear surgery, and it can occur with other inner ear disorders, allergies, or systemic disorders (such as diabetes or autoimmune disorders).

Although the underlying cause of endolymphatic hydrops is unknown, it is believed to result from abnormalities in the quantity, composition, and/or pressure of the endolymph, the fluid within the inner ear. Symptoms typical of endolymphatic hydrops include pressure or fullness in the ears, tinnitus (ringing or other noise in the ears), hearing loss, dizziness, and imbalance.

The diagnosis of endolymphatic hydrops is clinicaly based on the physician’s observations and on the patient's history, symptoms, and symptom pattern. The clinical diagnosis may be strengthened by the results of certain tests, including electrocochleography (ECoG) or audiometry.

Meniere's disease is characterized by sudden, violent attacks or episodes of vertigo, tinnitus, hearing loss, and aural fullness. Since secondary endolymphatic hydrops (SEH) results from an underlying disorder, the symptoms tend to be present more continuously, rather than occurring in spontaneous attacks. However, they are often less violent, and SEH may cause less damage to hearing and balance than does Meniere's disease.

A hydrops diet regimen which emphasizes eating a balanced diet in moderate amounts at regular intervals, minimizing the use of salts and sugars, and taking in plenty of fluids-often makes many people with SEH feel significantly better. A physician may prescribe diuretics. Other medications may be used to help with persistent dizziness, nausea, or vomiting.

Vestibular rehabilitation, a type of specialized physical therapy, can improve tolerance for activity, overall energy level, and symptoms of dizziness and imbalance. If dizziness and vertigo become intractable, the hair-cell structures of the inner ear may be selectively destroyed with the careful use of ototoxic (ear-poisoning) medication. In rare cases, surgery may be recommended.

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Labyrinthitis and Vestibular Neuritis

Labyrinthitis and vestibular neuritis are disorders resulting from an infection that inflames the inner ear or the vestibulo-cochlear nerve (the eighth cranial nerve), which connects the inner ear to the brain. Vertigo, dizziness, and difficulties with balance, vision, or hearing may result.

Infections of the inner ear are usually viral; less commonly, the cause is bacterial. Although the symptoms of bacterial and viral infections may be similar, the treatments are very different, so proper diagnosis by a physician is essential. Such inner ear infections are not the same as middle ear infections, which are the type of bacterial infections common in childhood affecting the area around the eardrum.

Neuritis (inflammation of the nerve) affects the vestibular branch of the vestibulo-cochlear nerve, resulting in dizziness or vertigo but no change in hearing. The term neuronitis is also used. Labyrinthitis (inflammation of the labyrinth) occurs when an infection affects both branches of the nerve, resulting in hearing changes as well as dizziness or vertigo.

An inner ear viral infection may be the result of a systemic viral illness (one affecting the rest of the body, such as infectious mononucleosis or measles); or the infection may be confined to the labyrinth or the vestibulo-cochlear nerve. Usually, only one ear is affected.

Symptoms of neuritis can be mild or severe, ranging from subtle dizziness to a violent spinning sensation (vertigo). They can also include nausea, vomiting, unsteadiness and imbalance, difficulty with vision, and impaired concentration. Sometimes the symptoms can be so severe that they affect the ability to sit up, stand, or walk. Labyrinthitis may produce the same symptoms, along with tinnitus (ringing or noises in the ear) and/or hearing loss.

The onset is usually very sudden, with severe dizziness developing abruptly during routine daily activities. In other cases, the symptoms are present upon awakening in the morning. After a period of gradual recovery that may last several weeks, some people are completely free of symptoms. Others have chronic dizziness, if the virus has damaged the vestibular nerve.

No specific tests exist to diagnose vestibular neuritis or labyrinthitis. When other illnesses have been ruled out, medications are often prescribed to control nausea and to suppress dizziness during the acute phase. Examples include Benadryl (diphenhydramine), Antivert (meclizine), Phenergen (promethazine hydrochloride), Ativan (lorazepam), and Valium (diazepam). Other medications that may be prescribed are steroids (e.g., prednisone), an antiviral drug (e.g., Acyclovir), or antibiotics (e.g., amoxicillin) if a middle ear infection is present.

If treated promptly, many inner ear infections cause no permanent damage. In some cases, however, permanent loss of hearing or damage to the vestibular system can occur. If symptoms of dizziness or imbalance persist for several months, vestibular rehabilitation exercises (a form of physical therapy) may be suggested in order to retrain the brain's ability to adjust to the vestibular imbalance, in a process known as compensation. A key component of successful adaptation is a dedicated effort to keep moving, despite the symptoms of dizziness and imbalance.

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Perilymph Fistula

A perilymph fistula is a tear or defect in the oval window and/or the round window, the small, thin membranes that separate the middle ear from the fluid-filled inner ear. When a fistula is present, changes in middle ear pressure will directly affect the inner ear, stimulating the balance and/or hearing structures and causing symptoms.

The symptoms of perilymph fistula may include dizziness, vertigo, imbalance, nausea, and vomiting. Some people experience ringing or fullness in the ears, and many notice a hearing loss. Most people with fistulas find that their symptoms get worse with changes in altitude (elevators, airplanes, travel over mountain passes) or air pressure (weather changes), as well as with exertion and activity.

Head trauma is the most common cause of fistulas. Fistulas may also develop after rapid or profound changes in intracranial or atmospheric pressure, such as may occur with SCUBA diving, aerobatic maneuvers in airplanes, weightlifting, or childbirth. Fistulas may be present from birth or may result from chronic, severe ear infections. Rarely, they appear to occur spontaneously.

History, physical examination, and vestibular and audiometric test results are used to assist in establishing the diagnosis of perilymph fistula. However, the only positive way the diagnosis can be confirmed is by performing a tympanotomy (operation) and directly viewing the area of the suspected fistula. In many cases, a fistula will heal itself with strict bed rest, to give the fistula a chance to close. If symptoms are severe and have not responded to bed rest, or if progressive hearing loss has occurred, surgical repair of the fistulas may be required.

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Acoustic Neuroma

An acoustic neuroma is a benign tumor on the vestibular portion of the eighth cranial nerve, which connects the inner ear to the brain. Both hearing and balance may be affected.

Acoustic neuromas are rare. Only about 2,000 cases are diagnosed in the United States each year.

Some acoustic neuromas cause a period of unsteadiness or imbalance. This imbalance can occur without other typical symptoms, such as one-sided hearing loss or intense ringing in the ear. Most acoustic neuromas are removed by microsurgery. Other options, including various types of radiation therapy (often called radiosurgery) are also available. Each type of treatment entails some risk of permanent change in hearing, balance, and facial motion. Some people may experience imbalance for several months after surgery.

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Ototoxicity ("ear poisoning") is due to drugs or chemicals that damage the inner ear or the vestibulo-cochlear nerve, which sends balance and hearing information from the inner ear to the brain. Ototoxicity can result in temporary or permanent disturbances of hearing, balance, or both.

Many chemicals have ototoxic potential, including over-the-counter drugs, prescription medications, and environmental chemicals. If you are taking any drugs on the advice of your physician, do not stop taking them just because you see them listed below. Speak with your doctor or other health care advisor about your concerns.

Substances that may cause ototoxicity include:

Aminoglycoside antibiotics, including gentamicin, streptomycin, kanamycin, tobramycin, neomycin, amikacin, netilmicin, dihydrostreptomycin, and ribostamycin. All members of this family are well known for their potential to cause permanent ototoxicity. They can enter the inner ear through the blood system, through inhalation, or via diffusion from the middle ear into the inner ear. They enter the blood stream in largest amounts when given intravenously (by IV).

Anti-neoplastics (anti-cancer drugs). Cisplatin is well known to cause hearing loss that is many times massive and permanent. Carboplatin has been implicated as well.

Environmental chemicals, including butyl nitrite, mercury, carbon disulfide, styrene, carbon monoxide, tin, hexane, toluene, lead, trichloroethylene, manganese, and xylene. Most are associated with hearing disturbances that may be permanent; mercury has also been linked to permanent balance problems.

Loop diuretics, including bumetanide (Bumex), ethacrynic acid (Edecrin), furosemide (Lasix), and torsemide (Demadex). These drugs cause ringing in the ears or decreased hearing that reverses when the drug is stopped. Note: Hydrochlorothiazide (HCTZ) and Maxide, diuretics commonly prescribed to people with Meniere's disease or other forms of endolymphatic hydrops, are not loop diuretics.

Aspirin and quinine products. These may cause temporary ototoxicity, particularly tinnitus, but may also reduce hearing.

Symptoms of ototoxicity vary considerably from drug to drug and person to person. They range from mild imbalance to total incapacitation, and from tinnitus to total hearing loss.

A bilateral (two-sided) vestibular loss usually doesn't produce intense vertigo, vomiting, and nystagmus but instead a headache, a feeling of ear fullness, imbalance to the point of being unable to walk, and a bouncing and blurring of vision (oscillopsia). It also produces inability to tolerate head movement, a wide-based gait (walking with the legs farther apart than usual), difficulty walking in the dark, a feeling of unsteadiness and actual unsteadiness while moving, lightheadedness, and severe fatigue. If the damage is severe, symptoms such as oscillopsia and problems with walking in the dark or with the eyes closed are not going to go away.

The diagnosis of ototoxicity is based upon the patient’s history, symptoms, and test results. There is no specific test; this makes a positive history for ototoxin exposure crucial to the diagnosis.

At present, there are no treatments that can reverse the damage. Currently available treatments are aimed at reducing the effect of the damage and rehabilitating function. Individuals with hearing loss may be helped with hearing aids, and those with profound bilateral losses have benefited from cochlear implants. In the case of lost balance function, physical therapy is of great value for many individuals. The aim is to help the brain become accustomed to the changed information from the inner ear and to assist the individual in developing other ways to maintain balance.

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Vestibular Migraine

Migraine, a disorder usually associated with headache, can cause several vestibular syndromes. Migraine is extremely common. Studies suggest that more than 20 million people in the United States suffer from migraine and that about 25 percent of these experience dizziness during attacks.

The International Headache Society classifies migraine disorders into several types. Migraine without aura consists of periodic headaches that are usually throbbing and one-sided, made worse by activity, and associated with nausea and increased sensitivity to light and noise. Vertigo can occur before, during, or separately from the episodes of migrainous headache. Migraine with aura, or classic migraine, is associated with short-lived symptoms (noises, flashes of light, tingling, numbness, vertigo, and others) known as the aura. These symptoms usually precede the headache and usually last 5 to 20 minutes. In a variation called migraine with prolonged aura, these symptoms may last a week. Migraine patients may experience migraine with aura on some occasions and migraine without aura on other occasions. Symptoms of basilar migraine include vertigo, tinnitus, decreased hearing, and ataxia (loss of coordination).

Several vestibular syndromes are caused by migraine. Benign recurrent vertigo of adults (not to be confused with BPPV, or benign paroxysmal positional vertigo) consists of spells of vertigo, occasionally with tinnitus but without hearing loss. Doctors must rule out other possible causes before making a diagnosis of migraine-induced vertigo. Benign paroxysmal vertigo of childhood (not to be confused with BPPV) consists of spells of imbalance and vertigo without hearing loss or tinnitus (ringing in the ears). The majority of cases occur between the ages of 1 and 4 but may occur up to age 10. Migrainous infarction or complicated migraine is a migraine with aura associated with a stroke (blood-flow problem resulting in cell death); one of the symptoms may be vertigo.

In addition to the syndromes caused by migraine, several vestibular disorders have been associated with migraine. Studies indicate that people with migraine are much more likely than other people to experience severe motion sickness and may be more likely to suffer from Meniere's disease or BPPV.

Stress, anxiety, hypoglycemia, fluctuating estrogen, certain foods, smoking, and other factors can trigger migraine. Vertigo and imbalance secondary to migraine usually respond to the same treatment used for migraine headaches. Treatment of migraine includes eliminating from the diet substances known to trigger migraine attacks, such as chocolate, nuts, cheese, red wine, and other foods. Medications may also be prescribed.

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Mal de Debarquement

Mal de debarquement literally means “sickness of disembarkment”. This term originally referred to the illusion of movement felt as an aftereffect of travel by ship or boat. Some experts now include other types of travel (such as by train and airplane) and situations with new and different movement patterns (such as reclining on a waterbed).

For a handful of people, this illusion of movement seems to last for long periods of time: weeks to months, even years after a voyage. Some physicians refer to it as mal de debarquement syndrome, reflecting that it is a collection of symptoms rather than a specific disease. There is no universal agreement among physicians about what mal de debarquement is or how to diagnose it. Not all doctors even agree that persistent mal de debarquement exists.

Leading explanations for the syndrome conclude that the problem is not in the inner ear and most likely occurs someplace in the balance areas of the brain. The brain adapts to the motion of the ship or other vehicle; but once the movement stops, the brain is unable to readapt once again. Why this ability to adapt would suddenly stop is not understood. One theory is that mal de debarquement is a migraine variant; long-lasting mal de debarquement is experienced by middle-aged woman more than by other groups, and more women than men experience migraines.

Symptoms of mal de debarquement include the sensation of bobbing, rocking, swaying, swinging, floating and/or tumbling. These may be accompanied by unsteadiness, disequilibrium, anxiety, difficulty concentrating, and a loss of self-confidence. The symptoms usually increase in enclosed spaces and when trying to be motionless such as when attempting to fall asleep in bed or when stopped at a traffic light. The symptoms improve during constant, steady movement such as experienced while in a moving car. Mal de debarquement does not include spinning vertigo, vomiting, cold sweat, ear pressure, ear pain, sound sensitivity, tinnitus, hearing loss or distortion, double vision, or bouncing vision.

Persistent mal de debarquement usually begins within hours of stopping the novel movement and resolves within about six to twelve months. There are also reports of it not resolving for years.

A physician diagnoses mal de debarquement by collecting a thorough history, conducting a physical examination, and doing tests to rule out other causes for the symptoms. For a diagnosis of mal de debarquement to be made, there must be a history of a ship voyage or other new movement, the return to a normal environment, and then the start of the symptoms. Symptoms start immediately, not weeks or months later.

At this time there appears to be no single highly successful treatment approach to mal de debarquement. Standard drugs given for motion sickness (including meclizine, diphenhydrinate, and scopolamine patches) seem to be ineffective. Some treatments suggested by physicians include walking while watching the horizon, vestibular rehabilitation therapy, diuretics, anti-seizure drugs, antidepressants of the tricyclic family, and benzodiazepines.

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Pediatric Vestibular Disorders

Vestibular disorders in children are generally considered uncommon. They are not as easily recognized as vestibular disorders in adults, in part because children cannot describe their symptoms as well.

Symptoms and signs that may indicate vestibular dysfunction in children include developmental and reflex delays, visual-spatial problems, hearing loss, tinnitus, motion sensitivity, abnormal movement patterns, clumsiness, decreased eye-hand and eye-foot coordination, ataxia, falls, nystagmus, seizures, dizziness, nausea, ear pressure, difficulty moving in the dark, behavioral changes, and/or delays in performance of developmental activities such as riding a bicycle, hopping, and stair climbing involving alternating left-right leg movements.

Possible causes include head-neck trauma, chronic ear infections, maternal drug or alcohol abuse during pregnancy, cytomegalovirus, immune-deficiency disorders, migraine with or without headache, meningitis, metabolic disorders (e.g., diabetes), ototoxic medications, neurological disorders (e.g., cerebral palsy, hydrocephalus), genetic syndromes (e.g., branchio-otorenal syndrome, Mondini dysplasia, Wallenberg syndrome), posterior brain tumors (e.g., malignant medullo-blastomas or the less frequently seen benign acoustic neuromas), and a family history of vertigo, motion sensitivity, hearing loss, or vestibular disorders. Dizziness can be the first symptom of depression in a teenager. Alcohol intoxication can produce dizziness, imbalance, staggering, and abnormal eye movements.

Children may also develop a vestibular disorder for no known reason. The underlying reasons often cannot be determined even with the most aggressive testing. This does not preclude successful treatment or recovery.

Children can experience the same vestibular disorders as adults. Benign paroxysmal positional vertigo (BPPV) in children is typically associated with physical trauma and can result from accidents, falls, or sports injuries. Infrequently, BPPV has also been observed following cochlear implantation. Vestibular neuritis or labyrinthitis occurs in children, as well as ototoxicity. Children that experience ototoxicity can have severe imbalance, falls, and visual-motor problems, including oscillopsia (bouncing vision).

Less common in children is Meniere's disease, enlarged vestibular aqueduct, perilymph fistula, autoimmune disease, and vascular insufficiencies.

In addition to all the vestibular disorders that adults are subject to, children have two of their own.

Childhood paroxysmal vertigo, often referred to as migraine equivalent, is typically seen in children 2-12 years old and is characterized by true spinning vertigo, nystagmus, nausea, and vomiting. Children tend to ”grow out of“ this condition, but it may progress into benign positional vertigo or migraine-associated vertigo in adulthood. Paroxysmal torticollis of infancy consists of head-tilt spells that may be associated with nausea, vomiting, pallor, agitation, and ataxia.

Evaluation and treatment: Age-specific techniques are used for assessment and treatment of vestibular dysfunction in children. A diagnostic work-up might include a history and physical exam, a hearing test, and possibly brain scans to rule out other pathologies. In addition, a vestibular therapist can help evaluate the child's ability to use the vestibular system for balance and visual-motor control, as well as test the child’s developmental reflexes that have control mechanisms in the vestibular system.

Using these results, the therapist develops vestibular-therapy exercises, which are tailored to the individual child. Children with vestibular disorders can respond well to such intervention. In fact, children typically respond more quickly than adults, because of their greater plasticity the ability of their neurological systems to more quickly compensate for and adapt to vestibular deficits. In addition, children tend to be less fearful of movement than adults, so they participate well in the balance and movement aspects of therapy. Vestibular therapy can be effective for reducing or eliminating vertigo, improving visual-motor control, improving balance and coordination, and promoting normal development in children with vestibular disorders.

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Aging, Balance and Dizziness

Balance: One of the leading health concerns for people over 60 is falling. Balance in walking and standing is dependent on many factors. The elderly have a higher risk of contracting many different kinds of diseases that can interfere with balance, including cataracts, glaucoma, diabetic retinopathy, and macular degeneration, which all affect vision; peripheral neuropathy, which affects position sense in the feet and legs; and vestibular-system degeneration.

Balance is also dependent on good muscle strength and joint mobility. A sedentary lifestyle and arthritis or other diseases of bones and muscles can compromise strength and mobility. Yet even healthy people over 65 appear to have more trouble than younger people in maintaining their balance on soft or uneven surfaces when visual cues are not available (e.g., in the dark).

Dizziness in the elderly can be a result of problems with the vestibular, central (brain-related), and vision systems, as well as from neuropathy, psychological causes, and unknown causes. Vestibular disorders, however, are thought to be the most common cause of dizziness in older people, responsible for approximately 50% of the reported dizziness in the elderly.

Until recently, relatively little was known about the consequences of aging for the vestibular system. Anatomical studies have shown that the number of nerve cells in the vestibular system grows smaller with age, beginning at about age 55. The loss becomes more severe as age progresses.

Of all vestibular disorders, benign paroxysmal positional vertigo (BPPV) is one of the most common. See the description of BPPV and treatment for it through vestibular rehabilitation therapy (balance-retraining exercises and maneuvers).

The ability to move about freely is an important factor in the quality of life of both younger and older people. A healthy vestibular system is vitally important to freedom of movement.

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Cervicogenic Dizziness

Neck pain often accompanies dizziness, but it may be difficult to tell whether the dizziness and the neck pain are related or just coincidental. In the 1950s, a clinical syndrome of disequilibrium and disorientation in patients with many different diagnoses of neck pathology�including cervical spondylosis, cervical trauma, and cervical arthritis�was introduced as cervical vertigo. Because true spinning vertigo is rarely associated with this syndrome, cervicogenic dizziness is a more accurate name for this syndrome.

Cervicogenic dizziness tends to be a controversial diagnosis, because there are no tests to confirm that it is the cause of the dizziness. The diagnosis is provided to people who have neck injury or pain as well as dizziness and in whom other causes of dizziness have been ruled out. Although no formal studies have been completed, true cervicogenic dizziness is thought to be rare.

People with cervicogenic dizziness tend to complain of dizziness that is worse during head movements or after maintaining one head position for a long time. The dizziness usually occurs after the neck pain and may be accompanied by a headache. The symptoms of dizziness usually last minutes to hours. People with cervicogenic dizziness may also complain of general imbalance that may increase with head movements and with movement in the environment.

An evaluation for cervicogenic dizziness involves a thorough medical evaluation. Testing of inner ear function is usually requested to ensure that the peripheral or central vestibular system is intact. A health care practitioner may perform a maneuver in which the body is turned while the head is held fixed to see if it causes nystagmus (eye movements) or dizziness to confirm the suspected diagnosis. This test can also be positive in healthy individuals.

Cervicogenic dizziness often occurs as a result of whiplash or head injury and is often seen in conjunction with brain injury or injury to the inner ear. The majority of patients improve with only treatment of the neck problem. Several studies have reported that approximately 75 percent of patients improve with conservative treatment of the neck such as medication, gentle mobilization, exercise, and instruction in proper posture and use of the neck.Others improve with treatment of the neck problem in addition to vestibular therapy.

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What is a cholesteatoma? A cholesteatoma is a skin growth that occurs in an abnormal location: the middle ear behind the eardrum. It is usually caused by repeated infection that causes an ingrowth of the skin of the eardrum. Cholesteatomas often take the form of a cyst or pouch that sheds layers of old skin that builds up inside the ear. Over time, the cholesteatoma can increase in size and destroy the surrounding delicate bones of the middle ear. Hearing loss, dizziness, and facial muscle paralysis are rare but can result from continued cholesteatoma growth.

How does it occur?

A cholesteatoma usually occurs because of poor eustachian tube function as well as infection in the middle ear. A rare congenital form of cholesteatoma (one present at birth) can occur in the middle ear and elsewhere, such as in the nearby skull bones. However, the type of cholesteatoma associated with ear infections is most common.

What are the symptoms?

Initially, the ear may drain, sometimes with a foul odor. As the cholesteatoma pouch or sac enlarges, it can cause a full feeling or pressure in the ear, along with hearing loss. (An ache behind or in the ear, especially at night, may cause significant discomfort.) Dizziness, or muscle weakness on one side of the face (the side of the infected ear) can also occur.


An examination by an otolaryngologist-head and neck surgeon can confirm the presence of a cholesteatoma. Initial treatment may consist of a careful cleaning of the ear, antibiotics, and eardrops. Therapy aims to stop drainage in the ear by controlling the infection. Large or complicated cholesteatomas usually require surgical treatment to protect the patient from serious complications.

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Enlarged Vestibular Aqueduct

The vestibular aqueduct (one on each side of the head) is a narrow bony canal extending from the middle compartment-vestibule-of the inner ear toward the brain. It houses the endolymphatic duct and sac along with a vein and artery.

If a vestibular aqueduct is greater than 1.5 millimeters in size (approximately the size of the head of a pin), it is considered to be an enlarged vestibular aqueduct (EVA). An enlarged endolymphatic duct and sac usually accompany EVA. The fluid-filled duct and sac are thought to help regulate the concentration of ions in the inner ear, which are important for initiating the transmission of sound and balance signals from the ear to the brain.


EVA seems to run in some families but not in others. It occurs more often in females than males. Genetic and as yet unknown environmental factors are thought to result in this disorder. EVA can be a symptom of Pendred syndrome (a genetic disorder causing childhood hearing loss), Mondini’s deformity (when the cochlea has only one or 1½ turns rather than the normal 2½), or branchio-otorenal syndrome (a genetic condition affecting the ears and the kidneys).


Hearing loss is commonly associated with enlarged vestibular aqueduct and is progressive with Pendred syndrome, sometimes resulting in total deafness. The hearing loss is generally sensorineural involving the cochlea and the nerves serving it.

EVA can also produce problems with balance, although vestibular symptoms can be difficult for a child to describe and thus may not always be reported. Symptoms described in the medical literature include episodic spinning vertigo, mild unsteadiness, trouble watching revolving objects, and decreased visual acuity, among others. In a young child, signs and symptoms may also include grabbing of the head and walking in circles.


An EVA diagnosis is made using standard hearing tests and high-resolution, thin-section computerized tomography of the temporal bone. Vestibular tests may also be useful in assessing the impact on balance.


Currently, no treatments can reverse or stop the progression of hearing and/or vestibular losses from EVA. People with EVAS are advised to avoid head blows and contact sports. Hearing aids or cochlear implantation may help. Vestibular rehabilitation therapy might also be helpful for managing imbalance and dizziness resulting from an enlarged vestibular aqueduct.

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Vestibular Hyperacusis

Hyperacusis is the perception of an unusual auditory sensitivity to some environmental noises or tones. It is an abnormal condition in which the complex electrical signals generated by sound vibrations are misinterpreted, confused, or exaggerated.

Symptoms of hyperacusis can range from a mild sense of unease to a complete loss of balance or upright posture with severe ear pain. In serious cases, it can cause seizure-like activity in the brain.

What is the difference between cochlear hyperacusis and vestibular hyperacusis? With cochlear hyperacusis, subjects feel ear pain, discomfort, annoyance, or some other emotional reaction when certain sounds are heard, including those that are very soft or high-pitched. In vestibular hyperacusis, exposure to sound can result in falling or a loss of balance or postural control. Such disturbances have been called by various names, including Tullio's syndrome and audiogenic seizure disorder. Some of the same reactions as with cochlear hyperacusis can also occur, along with sudden severe vertigo or nausea. In some cases, vestibular hyperacusis can affect the autonomic system and cause problems such as loss of consciousness, mental confusion, nausea, or extreme fatigue. In both cochlear and vestibular hyperacusis, headache is common.

Causes: Hyperacusis can be associated with auto-immune disorders, traumatic brain injury, metabolic disorders, and other conditions, although it is often ascribed to psychological conditions rather than being recognized as a physiologic symptom of cochlear or vestibular damage. The physiologic conditions underlying these symptoms cannot be identified with certainty because of difficulties involved with studying the very small inner ear structures without damaging them.

A suspected cause of cochlear hyperacusis involves a loss of the regulatory function provided by the system that conducts impulses along the auditory neural pathways. Thus, for example, the sound of a passing car might be interpreted as comparable to the roar of a jet engine. Other possible causes involve brain-chemistry dysfunction or head trauma that damages the chain of tiny bones in the middle ear that amplify sound and help transmit vibrations to the inner ear fluid.

In vestibular hyperacusis, damage to the nerve cells in the balance system is suspected, possibly from head injury, metabolic disruptions due to chemical ingestions (e.g., medications or anesthesia), or circulatory changes due to heart disease or artery blockages. In addition, autoimmune disease, which can be triggered by many different causes, can harm the balance organ.

Testing and treatment: While special audiologic tests can reveal the presence and severity of cochlear hyperacusis, and help define treatment, diagnosis and treatment of vestibular hyperacusis is less defined. When vestibular hyperacusis is recognized, the treatment protocols vary widely and have included a low-salt diet combined with anti-nausea drugs, and the introduction of anti-inflammatory medicines directly into the cochlear/vestibular system using catheters.

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Autoimmune Inner Ear Disease

What is autoimmunity?

When a virus attacks, the immune system defends the body. The defense capabilities of a malfunctioning immune system can harm the body by mistaking and attacking the body’s own cells as if they were invading viruses or germs. This is called autoimmunity.

In general, autoimmune disorders occur more frequently in women than men and less frequently in children and the elderly.

What is autoimmune inner ear disease?

The immune system can attack the whole body or just certain systems within the body, including the ear. Even if the ear is not being directly attacked, debris created by an autoimmune reaction in one part of the body can be transported to the ear by circulation, and hence cause problems to the ear. When the ear is attacked, the progression of damage and functional loss can be rapid.

Some autoimmune disorders that can affect the ear include Cogan’s syndrome, relapsing polychondritis, polyarteritis nodosa, Wegener’s granulomatosis, systemic lupus erythematosus, ulcerative colitis, Sjogren’s syndrome, and rheumatoid arthritis.


The most prominent symptom of autoimmune inner ear disease is bilateral asymmetric progressive/fluctuating sensorineural hearing loss, typically occurring over several months. Sometimes the progression can be over several years. The presence of vertigo and other symptoms typically related to vestibular loss depends on the degree of loss and whether the damage has triggered a problem with fluctuating function (for example, if endolymphatic hydrops developed from the autoimmune reaction). The symptoms of autoimmune problems can be similar, even indistinguishable, from other vestibular disorders; a Meniere�s syndrome is sometimes present.


Diagnosing an autoimmune disorder as the cause of inner ear symptoms can be difficult. Aside from a history of other systemic autoimmune disorders and supportive blood tests, sometimes the diagnosis is made only if hearing improvement occurs in response to drug treatment.


An early diagnosis is important because treatment can be effective in stopping the progression or reversing the damage.

The standard treatment for autoimmune reactions is immunosuppressive medication, sometimes delivered as long term therapy. Such medications have body-wide effects and include steroids, chemotherapy agents, anti-transplant rejection drugs, and the newer anti-tumor, necrosis-factor drugs. Because a rheumatologist has extensive training and experience in these treatments, they are often called on to manage the drug treatment in collaboration with the otolaryngologist or neurotologist.

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Superior Canal Dehiscence Syndrome

Superior canal dehiscence syndrome (SCD) results from an opening (dehiscence) in the bone overlying the superior (uppermost) semicircular canal within the inner ear. With this dehiscence, the fluid in the membranous superior canal (which is located within the tubular cavity of the bony canal) can be displaced by sound and pressure stimuli.

There are normally only two points of increased compliance (yielding to pressure) in the inner ear: the oval window, through which sound energy is transmitted into the inner ear via the stapes bone; and the round window, through which sound energy is dissipated from the inner ear after traveling around the cochlea. SCD creates a third mobile window into the inner ear. Signs and symptoms of SCD result from the physiological consequences of this third window.

Vestibular and/or auditory signs and symptoms can occur in SCD. Vertigo and oscillopsia (the apparent motion of objects that are known to be stationary) evoked by loud noises and/or by maneuvers that change middle-ear or intracranial pressure (such as coughing, sneezing, or straining). Persons with SCD may experience a feeling of constant disequilibrium and imbalance, and may perceive that objects are moving in time with their pulse (pulsatile oscillopsia). Auditory manifestations of SCD may include autophony (increased resonance of one’s own voice), hypersensitivity to bone-conducted sounds, and an apparent conductive hearing loss revealed on audiometry.

The diagnosis of SCD is made based upon characteristic symptoms, specific findings on clinical examination, CT imaging, and findings on vestibular evoked myogenic potentials (VEMP) testing. The diagnosis should never be made exclusively on the basis of CT findings.

For many patients, avoidance of provocative stimuli such as loud noises may be sufficient treatment. For those patients who are debilitated by their symptoms, surgical plugging of the superior canal can be very beneficial in alleviating or substantially reducing the symptoms and signs.

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