Syndromes Primarily Involving Vestibular Function

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Conditions that involve vestibular function can be separated into peripheral (otological vertigo) and central subgroups. Patients with these syndromes present clinically with a combination of vertigo and ataxia. Practically, there are far more cases of otological vertigo than central vertigo, and for this reason, in clinical practice, a detailed understanding of otological vertigo is essential.


Benign paroxysmal positional vertigo is the cause of half of all cases of otological vertigo; it accounts for about 20 percent of all patients with vertigo. Benign paroxysmal positional vertigo is diagnosed by the history of positional vertigo with a typical nystagmus pattern (a burst of upbeating/torsional nystagmus) on Dix-Hallpike positional testing. Symptoms are precipitated by movement or a position change of the head or body. Getting out of bed or rolling over in bed are the most common "problem" motions. A burst of nystagmus can often be provoked by placing the head in positions wherein the posterior canal is made vertical in space, and ENG testing may be helpful in documenting this condition. Benign paroxysmal positional vertigo is usually a straightforward clinical diagnosis. Ordinarily there is no need to obtain neuroradiological tests, audiometric testing, or posturography.

It is currently thought that BPPV is caused by the presence of free debris, possibly otoconia, within the semicircular canals, which is dislodged from the otolith organs by trauma, infection, or degeneration (.Fig 12..-.7 ). The otoconial debris can move about by changes in head position, causing vertigo and nystagmus when the debris tumble through the semicircular canals. The duration of symptoms is brief, because dizziness occurs only while the debris shifts position. Physical treatments based on the manipulation of head are the most effective remedies for BPPV. These maneuvers reposition the otolithic debris to an insensitive location within the inner ear. y


Vestibular neuritis is a self-limited otological condition. Patients present with vertigo, nausea, ataxia, and nystagmus. Most cases of vestibular neuritis are monophasic. Hearing is not impaired, and when there are similar symptoms with abnormal hearing, the syndrome is termed labyrinthitis. A strong nystagmus is seen acutely, and Frenzel's

Figure 12-7 Debris hypothesis of benign paroxysmal positional vertigo. Otoconia displaced from the utricle gravitate to the most dependent parts of the inner ear.

goggles are particularly useful in seeing these eye movements. Vestibular neuritis is thought to be caused by viral infections involving the vestibular portion of the eighth nerve.

Similar symptoms may be seen with other etiologies. Meniere's disease is usually recognized by the episodic pattern (see later). Herpes simplex virus infection of the vestibular nerve is recognized by a combination of ear pain and the presence of vesicles on the external canal. Acoustic neuroma (discussed later) is recognized by a slower course and the occurrence of hearing loss. Vascular disorders such as a labyrinthine artery infarction are generally impossible to exclude, and their diagnosis is suggested by an identical symptom complex combined with vascular risk factors.

No laboratory testing is needed in straightforward cases. When a central disorder is suspected in the setting of multiple cerebrovascular risk factors or neurological diseases, however, further laboratory testing may be helpful to confirm the anatomical diagnosis. Electronystagmography testing often reveals a significantly decreased caloric response on one side as well as spontaneous nystagmus. Rotational testing is not necessary, but when obtained, it typically shows reduced gain and increased phase lead. Posturography is also not necessary, but results are typically abnormal, indicating that balance is impaired.

In vestibular neuritis, severe distress associated with constant vertigo, nausea, and malaise usually lasts 2 or 3 days, and less intense symptoms ordinarily persist for

1 or 2 weeks. The treatment strategy involves the use of vestibular suppressants and antiemetics (.Tables 12-8 and 12-9 ). Roughly 10 percent of patients may take as long as 2 months for the condition to improve substantially. These patients usually have a significant fixed vestibular paresis combined with central dysfunction that slows their compensation. For example, patients with alcoholic cerebellar degeneration or persons of advanced age may recover much more slowly. Such patients often benefit from visual- vestibular exercises.

Vestibular exercise instructions may be given to patients in the form of a handout. y These exercises are done three times daily, moving from the easier procedures to more difficult ones, as recovery ensues. Specialized physical therapy programs are also available in which individualized therapy can be offered and supervision provided, when appropriate. It should also be noted that numerous avocational activities serve well to promote vestibular compensation, and depending on the abilities and interests of patients, clinicians may prescribe golf, bowling, racquetball, bicycling, or even t'ai chi.


Acoustic neuromas and other tumors such as meningiomas, which can appear at the cerebellopontine angle, usually display asymmetrical sensorineural hearing loss. Usually, patients in the fifth or greater decade present with mild vertigo or ataxia, accompanied by a significant asymmetrical hearing loss. Generally, there are no other physical examination abnormalities, and facial and sixth nerve functions are ordinarily normal.

If the hearing loss is minor, an audiogram may be performed within 6 months. If hearing loss progressively worsens, an MRI scan should be pursued. If a tumor is identified and is small, or the patient is reluctant to have surgery, the tumor may be followed with periodical evaluations. MRI should be repeated every year, more frequently if there is a substantial change in hearing. In many instances, lesions remain stable over many years and surgery can be avoided. Gamma knife treatment is an emerging modality and may also be used when surgery is refused or when the patient is a poor surgical risk.


Classic Meniere's disease presents as a quadrad of paroxysmal symptoms, including tinnitus, monaural fullness, fluctuating hearing, and episodic vertigo. This clinical picture is sometimes called the "hydrops" symptom complex, inferring that the mechanism is related to dilation and




Adverse Reactions

Pharmacologie Class and


Meclizine (Antivert,

12.5-50 mg every 4-6 hours

Sedating, precautions in prostatic enlargement, glaucoma




Lorazepam (Ativan)

0.5 mg twice daily

Mildly sedating


Drug dependency

Clonazepam (Klonopin)

0.5 mg twice daily

Mildly sedating


Drug dependency


0.5 mg patch every 3 days

Topical allergy with chronic use. Precautions in glaucoma,



tachyarrhythmias, prostatic enlargement

Dimenhydrinate (Dramamine)

Diazepam (Valium)

5G mg every 4-6 hours

2-10 mg (1 dose) given acutely orally, intramuscularly, or intravenously

Same as meclizine Sedating

Respiratory depressant Drug dependency Precaution in glaucoma

Doses listed are used in adults Drugs arranged in order of preference.






Usual Dose (Adults)

Adverse Reactions

Pharmacological Class

Droperidol (Inapsine)

2.5 or 5 mg sublingual or intramuscularly every 12 hours


Dopamine antagonist



Meclizine (Antivert, Bonine)

12.5-50 mg every 4-6 hours orally


Antihistamine and

Precautions in glaucoma, prostate



Metoclopramide (Reglan)

10 mg orally three times daily or 10 mg intramuscularly

Restlessness or drowsiness

Dopamine antagonist


Ondansetron (Zofran)

4-8 mg po single dose


5-HT3 antagonist


5 mg or 10 mg intramuscularly or orally every 6-12 hours or 25




rectal every 12 hours


Promethazine (Phenergan)

12.5-25 mg orally every 6-8 hours or 12.5-25 mg rectal every 12




12.5 mg intramuseularly every 6-8 hours


Trimethobenzamide (Tigan)

250 mg orally three times daily or 200 mg intramuscularly three


Similar to phenothiazine

times daily


Thiethylperazine (Torecan)

10 mg orally, up to three times daily or 2 ml intramuscularly, up to



three times daily

Doses listed are used in adults.

rupture of the endolymphatic compartment of the inner ear. The tinnitus is characteristically of two types. Between attacks the tinnitus is characteristically a ringing noise (about 75 percent of the population has ringing tinnitus from time to time). During an attack, the tinnitus becomes a multifrequency noise such as a roar, hiss, or buzz. Patients also generally complain of monaural fullness, a sensation as if the ear were full of water, beginning a day or two before an attack. Hearing is normal at the onset of the condition, but with each attack a low-frequency sensorineural reduction in hearing appears (see FigureJ.2-5 ), and then it usually resolves a day or two later. After many attacks, hearing begins to decline and involves the high frequencies. Ultimately, many individuals with Meniere's disease develop permanent sensorineural pattern deafness.

The clinical picture of Meniere's disease varies widely, with some patients developing deafness with their first attack and others retaining normal hearing after several decades of repeated attacks. Variants of Meniere's disease include a form that follows head injury (labyrinthine concussion or delayed endolymphatic hydrops), and a bilateral form attributed to autoantibodies or genetic predisposition.

The diagnosis of classic Meniere's disease can be made purely by history, but most commonly it is made by combining a history of episodic vertigo and hearing symptoms with audiometric documentation of a fluctuating low-tone sensorineural hearing loss. Electrocochleography may be useful in cases when the history is not classic. It is conventional practice to obtain several blood tests including fluorescent treponemal antibody, antinuclear antibody, complete blood count, and fasting blood glucose after diagnosing Meniere's disease to identify specific treatable causes.

In the treatment of Meniere's disease, vestibular suppressants and antiemetics are used in a way similar to that described for vestibular neuritis (see T§b!e.s...12:8 and 12.-9 ). Because bouts generally last only 2 hours, acute treatment is usually episodic. Often patients can anticipate an attack and can start taking an antiemetic and/or vestibular suppressant before their full-blown symptoms occur. It is presently generally accepted that reduction of salt intake with a no-added-salt diet and daily use of a salt-wasting diuretic is helpful in reducing the number and intensity of spells over the long term.

Effective surgical treatment of Meniere's disease is based on procedures that destroy vestibular function. Three procedures are commonly used today, including labyrinthectomy, selective vestibular nerve section, and transtympanic gentamicin treatment. Gentamicin treatment is presently growing rapidly in popularity.


In neurological practice, central vertigo typically makes up only about 25 percent of diagnoses of patients presenting with vertigo, because otological vertigo and vertigo of unknown cause are much more frequent (.Table 12-10 ). Stroke and transient ischemic attacks account for one third of cases of central vertigo. Vertigo attributed to vertebrobasilar migraine accounts for another 15 percent of cases. A large number of individual miscellaneous neurological disorders such as seizures, multiple sclerosis, and the Arnold-Chiari malformation make up the remainder.


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