Treatment of Vertigo



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Am Fam Physician. 2005 Mar 15;71(6):1115-1122.

  Patient Information Handout

Vertigo is the illusion of motion, usually rotational motion. As patients age, vertigo becomes an increasingly common presenting complaint. The most common causes of this condition are benign paroxysmal positional vertigo, acute vestibular neuronitis or labyrinthitis, Ménière’s disease, migraine, and anxiety disorders. Less common causes include vertebrobasilar ischemia and retrocochlear tumors. The distinction between peripheral and central vertigo usually can be made clinically and guides management decisions. Most patients with vertigo do not require extensive diagnostic testing and can be treated in the primary care setting. Benign paroxysmal positional vertigo usually improves with a canalith repositioning procedure. Acute vestibular neuronitis or labyrinthitis improves with initial stabilizing measures and a vestibular suppressant medication, followed by vestibular rehabilitation exercises. Ménière’s disease often responds to the combination of a low-salt diet and diuretics. Vertiginous migraine headaches generally improve with dietary changes, a tricyclic antidepressant, and a beta blocker or calcium channel blocker. Vertigo associated with anxiety usually responds to a selective serotonin reuptake inhibitor.

Vertigo, a type of dizziness, is the illusion of motion, usually rotational motion. Associated symptoms include nausea, emesis, and diaphoresis. Vertigo should be distinguished from other types of dizziness, such as imbalance (dysequilibrium) and lightheadedness (presyncope). Most cases of vertigo can be diagnosed clinically and managed in the primary care setting.

Strength of Recommendations

Key clinical recommendation Label References

The canalith repositioning procedure (Epley maneuver) is recommended in patients with benign paroxysmal positional vertigo.

A

18,19,20

The modified Epley maneuver also is effective in patients with benign paroxysmal positional vertigo.

B

16

Vestibular suppressant medication is recommended for symptom relief in patients with acute vestibular neuronitis.

C

6,7,8

Vestibular exercises are recommended for more rapid and complete vestibular compensation in patients with acute vestibular neuronitis.

B

14

Treatment with a low-salt diet and diuretics is recommended for patients with Ménière’s disease and vertigo.

B

23,24,25

Effective treatments for vertiginous migraine include migraine prophylaxis (e.g., tricyclic antidepressants, beta blockers, calcium channel blockers), migraine-abortive medications (e.g., sumatriptan [Imitrex]), and vestibular rehabilitation exercises.

B

13,30,31,32

Selective serotonin reuptake inhibitors can relieve vertigo in patients with anxiety disorders. Because of side effects, slow titration is recommended.

B

34


A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, opinion, or case series. See page 1046 for more information.

Strength of Recommendations

View Table

Strength of Recommendations

Key clinical recommendation Label References

The canalith repositioning procedure (Epley maneuver) is recommended in patients with benign paroxysmal positional vertigo.

A

18,19,20

The modified Epley maneuver also is effective in patients with benign paroxysmal positional vertigo.

B

16

Vestibular suppressant medication is recommended for symptom relief in patients with acute vestibular neuronitis.

C

6,7,8

Vestibular exercises are recommended for more rapid and complete vestibular compensation in patients with acute vestibular neuronitis.

B

14

Treatment with a low-salt diet and diuretics is recommended for patients with Ménière’s disease and vertigo.

B

23,24,25

Effective treatments for vertiginous migraine include migraine prophylaxis (e.g., tricyclic antidepressants, beta blockers, calcium channel blockers), migraine-abortive medications (e.g., sumatriptan [Imitrex]), and vestibular rehabilitation exercises.

B

13,30,31,32

Selective serotonin reuptake inhibitors can relieve vertigo in patients with anxiety disorders. Because of side effects, slow titration is recommended.

B

34


A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, opinion, or case series. See page 1046 for more information.

Vestibular Function and Vertigo

Vertigo results from acute unilateral vestibular lesions that can be peripheral (labyrinth or vestibular nerve) or central (brainstem or cerebellum). In contrast, tumors and ototoxic medications produce slowly progressive unilateral or bilateral lesions. Lesions that progress slowly or processes that affect both vestibular apparatuses equally usually do not result in vertigo.

Diagnosis of Vertigo

Because vertigo can have multiple concurrent causes (especially in older patients), a specific diagnosis can be elusive. The duration of vertiginous episodes and the presence or absence of auditory symptoms can help narrow the differential diagnosis (Table 1).1 Psychiatric disorders, motion sickness, serous otitis media, cerumen impaction, herpes zoster, and seizure disorders also can present with dizziness.

TABLE 1

Differential Diagnosis of Vertigo

Disorder Duration of episodes Auditory symptoms Prevalence Peripheral or central vertigo

Benign paroxysmal positional vertigo

Seconds

No

Common

Peripheral

Perilymphatic fistula (head trauma, barotrauma)

Seconds

Yes

Uncommon

Peripheral

Vascular ischemia: transient ischemic attack

Seconds to hours

Usually not

Uncommon

Central or peripheral*

Ménière’s disease

Hours

Yes

Common

Peripheral

Syphilis

Hours

Yes

Uncommon

Peripheral

Vertiginous migraine

Hours

No

Common

Central

Labyrinthine concussion

Days

Yes

Uncommon

Peripheral

Labyrinthitis

Days

Yes

Common

Peripheral

Vascular ischemia: stroke

Days

Usually not

Uncommon

Central or peripheral*

Vestibular neuronitis

Days

No

Common

Peripheral

Anxiety disorder

Variable

Usually not

Common

Unspecified

Acoustic neuroma

Months

Yes

Uncommon

Peripheral

Cerebellar degeneration

Months

No

Uncommon

Central

Cerebellar tumor

Months

No

Uncommon

Central

Multiple sclerosis

Months

No

Uncommon

Central

Vestibular ototoxicity

Months

Yes

Uncommon

Peripheral


*—Vertigo can be caused by vascular ischemia in the central vertebrobasilar circulation or the peripheral circulation to the vestibular nerve and labyrinth.1

TABLE 1   Differential Diagnosis of Vertigo

View Table

TABLE 1

Differential Diagnosis of Vertigo

Disorder Duration of episodes Auditory symptoms Prevalence Peripheral or central vertigo

Benign paroxysmal positional vertigo

Seconds

No

Common

Peripheral

Perilymphatic fistula (head trauma, barotrauma)

Seconds

Yes

Uncommon

Peripheral

Vascular ischemia: transient ischemic attack

Seconds to hours

Usually not

Uncommon

Central or peripheral*

Ménière’s disease

Hours

Yes

Common

Peripheral

Syphilis

Hours

Yes

Uncommon

Peripheral

Vertiginous migraine

Hours

No

Common

Central

Labyrinthine concussion

Days

Yes

Uncommon

Peripheral

Labyrinthitis

Days

Yes

Common

Peripheral

Vascular ischemia: stroke

Days

Usually not

Uncommon

Central or peripheral*

Vestibular neuronitis

Days

No

Common

Peripheral

Anxiety disorder

Variable

Usually not

Common

Unspecified

Acoustic neuroma

Months

Yes

Uncommon

Peripheral

Cerebellar degeneration

Months

No

Uncommon

Central

Cerebellar tumor

Months

No

Uncommon

Central

Multiple sclerosis

Months

No

Uncommon

Central

Vestibular ototoxicity

Months

Yes

Uncommon

Peripheral


*—Vertigo can be caused by vascular ischemia in the central vertebrobasilar circulation or the peripheral circulation to the vestibular nerve and labyrinth.1

The physical examination should include measurements of orthostatic vital signs and an otoscopic examination. The neurologic examination should include the Dix-Hallpike maneuver to differentiate peripheral from central vertigo2,3  (Figure 1 and Table 23,4).

Figure 1.

Dix-Hallpike maneuver (used to diagnose benign paroxysmal positional vertigo). This test consists of a series of two maneuvers: With the patient sitting on the examination table, facing forward, eyes open, the physician turns the patient’s head 45 degrees to the right (A). The physician supports the patient’s head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table. The patient remains in this position for 30 seconds (B). Then the patient returns to the upright position and is observed for 30 seconds. Next, the maneuver is repeated with the patient’s head turned to the left. A positive test is indicated if any of these maneuvers provide vertigo with or without nystagmus.

View Large


Figure 1.

Dix-Hallpike maneuver (used to diagnose benign paroxysmal positional vertigo). This test consists of a series of two maneuvers: With the patient sitting on the examination table, facing forward, eyes open, the physician turns the patient’s head 45 degrees to the right (A). The physician supports the patient’s head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table. The patient remains in this position for 30 seconds (B). Then the patient returns to the upright position and is observed for 30 seconds. Next, the maneuver is repeated with the patient’s head turned to the left. A positive test is indicated if any of these maneuvers provide vertigo with or without nystagmus.


Figure 1.

Dix-Hallpike maneuver (used to diagnose benign paroxysmal positional vertigo). This test consists of a series of two maneuvers: With the patient sitting on the examination table, facing forward, eyes open, the physician turns the patient’s head 45 degrees to the right (A). The physician supports the patient’s head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table. The patient remains in this position for 30 seconds (B). Then the patient returns to the upright position and is observed for 30 seconds. Next, the maneuver is repeated with the patient’s head turned to the left. A positive test is indicated if any of these maneuvers provide vertigo with or without nystagmus.

TABLE 2

Clues to Distinguish Between Peripheral and Central Vertigo

Clues Peripheral vertigo Central vertigo

Findings on Dix-Hallpike maneuver

Latency of symptoms and nystagmus

2 to 40 seconds

None

Severity of vertigo

Severe

Mild

Duration of nystagmus

Usually less than 1 minute

Usually more than 1 minute

Fatigability*

Yes

No

Habituation†

Yes

No

Other findings

Postural instability

Able to walk; unidirectional instability

Falls while walking; severe instability

Hearing loss or tinnitus

Can be present

Usually absent

Other neurologic symptoms

Absent

Usually present


*—Response remits spontaneously as position is maintained.

† —Attenuation of response as position repeatedly is assumed.

Information from references 3 and 4.

TABLE 2   Clues to Distinguish Between Peripheral and Central Vertigo

View Table

TABLE 2

Clues to Distinguish Between Peripheral and Central Vertigo

Clues Peripheral vertigo Central vertigo

Findings on Dix-Hallpike maneuver

Latency of symptoms and nystagmus

2 to 40 seconds

None

Severity of vertigo

Severe

Mild

Duration of nystagmus

Usually less than 1 minute

Usually more than 1 minute

Fatigability*

Yes

No

Habituation†

Yes

No

Other findings

Postural instability

Able to walk; unidirectional instability

Falls while walking; severe instability

Hearing loss or tinnitus

Can be present

Usually absent

Other neurologic symptoms

Absent

Usually present


*—Response remits spontaneously as position is maintained.

† —Attenuation of response as position repeatedly is assumed.

Information from references 3 and 4.

No laboratory testing is absolutely indicated in the work-up of patients with vertigo. If hearing loss is suspected, complete audiometric testing can help distinguish vestibular pathology from retrocochlear pathology (e.g., acoustic neuroma).

Brain imaging is warranted if a tumor or stroke is suspected. The American College of Radiology5 recommends magnetic resonance imaging with contrast medium when a patient presents with acute vertigo and sensorineural hearing loss. Magnetic resonance angiography can be used to evaluate the vertebrobasilar circulation.

General Treatment Principles

MEDICATIONS

Medications are most useful for treating acute vertigo that lasts a few hours to several days (Table 3).6,7 They have limited benefit in patients with benign paroxysmal positional vertigo, because the vertiginous episodes usually last less than one minute. Vertigo lasting more than a few days is suggestive of permanent vestibular injury (e.g., stroke), and medications should be stopped to allow the brain to adapt to new vestibular input.

TABLE 3

Medications Commonly Used In Patients with Acute Vertigo and Associated Nausea and Emesis

Medication Dosage Sedation Antiemesis Pregnancy category

Meclizine* (Antivert)

12.5 to 50 mg orally every 4 to 8 hours

++

+

B

Dimenhydrinate* (Dramamine)

25 to 100 mg orally, IM, or IV every 4 to 8 hours

+

++

B

Diazepam (Valium)

2 to 10 mg orally or IV every 4 to 8 hours

++

+

D

Lorazepam (Ativan)

0.5 to 2 mg orally, IM, or IV every 4 to 8 hours

++

+

D

Metoclopramide (Reglan)

5 to 10 mg orally every 6 hours

+

+++

B

5 to 10 mg by slow IV every 6 hours

Prochlorperazine (Compazine)

5 to 10 mg orally or IM every 6 to 8 hours

+

+++

C

25 mg rectally every 12 hours

5 to 10 mg by slow IV over 2 minutes

Promethazine (Phenergan)

12.5 to 25 mg orally, IM, or rectally every

+++

++

C

4 to 12 hours


*—Available over the counter.

+ = mild; ++ = moderate; +++ = prominent; IM = intramuscular; IV = intravenous.

Information from references 6 and 7.

TABLE 3   Medications Commonly Used In Patients with Acute Vertigo and Associated Nausea and Emesis

View Table

TABLE 3

Medications Commonly Used In Patients with Acute Vertigo and Associated Nausea and Emesis

Medication Dosage Sedation Antiemesis Pregnancy category

Meclizine* (Antivert)

12.5 to 50 mg orally every 4 to 8 hours

++

+

B

Dimenhydrinate* (Dramamine)

25 to 100 mg orally, IM, or IV every 4 to 8 hours

+

++

B

Diazepam (Valium)

2 to 10 mg orally or IV every 4 to 8 hours

++

+

D

Lorazepam (Ativan)

0.5 to 2 mg orally, IM, or IV every 4 to 8 hours

++

+

D

Metoclopramide (Reglan)

5 to 10 mg orally every 6 hours

+

+++

B

5 to 10 mg by slow IV every 6 hours

Prochlorperazine (Compazine)

5 to 10 mg orally or IM every 6 to 8 hours

+

+++

C

25 mg rectally every 12 hours

5 to 10 mg by slow IV over 2 minutes

Promethazine (Phenergan)

12.5 to 25 mg orally, IM, or rectally every

+++

++

C

4 to 12 hours


*—Available over the counter.

+ = mild; ++ = moderate; +++ = prominent; IM = intramuscular; IV = intravenous.

Information from references 6 and 7.

A wide variety of medications are used to treat vertigo and the frequently concurrent nausea and emesis. These medications exhibit various combinations of acetylcholine, dopamine, and histamine receptor antagonism. The American Gastroenterological Association recommends anticholinergics and antihistamines for the treatment of nausea associated with vertigo or motion sickness.8

Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the vestibular system.6 Benzodiazepines enhance the action of GABA in the central nervous system (CNS) and are effective in relieving vertigo and anxiety.

Older patients are at particular risk for side effects of vestibular suppressant medications (e.g., sedation, increased risk of falls, urinary retention). These patients also are more likely to experience drug interactions (i.e., additive effects with other CNS depressants).

VESTIBULAR REHABILITATION EXERCISES

Vestibular rehabilitation exercises commonly are included in the treatment of vertigo9,10 (see patient information handout). These exercises train the brain to use alternative visual and proprioceptive cues to maintain balance and gait. It is necessary for a patient to reexperience vertigo so that the brain can adapt to a new baseline of vestibular function. After acute stabilization of the patient with vertigo, use of vestibular suppressant medications should be minimized to facilitate the brain’s adaptation to new vestibular input.

A randomized, controlled trial (RCT)11 of 143 primary care patients with dizziness and vertigo showed that vestibular rehabilitation exercises improved nystagmus, postural control, movement-provoked dizziness, and subjective indexes of symptoms and distress. Another RCT12 evaluated the effectiveness of home vestibular rehabilitation in patients with chronic vertigo with a peripheral vestibular etiology. This trial12 showed a significant reduction of vertigo and an increase in the ability to perform activities of daily living independently.

A retrospective case series13 assessed the efficacy of physical therapy in patients who had vestibular and balance disorders with or without a history of migraine. Both groups showed significant alleviation of dizziness and improvement of balance and gait. Vestibular exercises also have been shown to improve postural control during the first month after acute unilateral vestibular lesions resulting from vestibular neuronitis.14

Treatment of Specific Disorders

BENIGN PAROXYSMAL POSITIONAL VERTIGO

Benign paroxysmal positional vertigo is caused by calcium debris in the semicircular canals (canalithiasis), usually the posterior canal. Medications generally are not recommended for the treatment of this condition.

The vertigo improves with head rotation maneuvers that displace free-moving calcium deposits back to the vestibule. Maneuvers include the canalith repositioning procedure or Epley maneuver15 and the modified Epley maneuver16 (Figure 2). The modified Epley maneuver can be performed at home.

Figure 2.

Epley maneuver. The patient sits on the examination table, with eyes open and head turned 45 degrees to the right (A). The physician supports the patient’s head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table (B). The physician turns the patient’s head 90 degrees to the left side. The patient remains in this position for 30 seconds (C). The physician turns the patient’s head an additional 90 degrees to the left while the patient rotates his or her body 90 degrees in the same direction. The patient remains in this position for 30 seconds (D). The patient sits up on the left side of the examination table. (E) The procedure may be repeated on either side until the patient experiences relief of symptoms.

View Large


Figure 2.

Epley maneuver. The patient sits on the examination table, with eyes open and head turned 45 degrees to the right (A). The physician supports the patient’s head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table (B). The physician turns the patient’s head 90 degrees to the left side. The patient remains in this position for 30 seconds (C). The physician turns the patient’s head an additional 90 degrees to the left while the patient rotates his or her body 90 degrees in the same direction. The patient remains in this position for 30 seconds (D). The patient sits up on the left side of the examination table. (E) The procedure may be repeated on either side until the patient experiences relief of symptoms.


Figure 2.

Epley maneuver. The patient sits on the examination table, with eyes open and head turned 45 degrees to the right (A). The physician supports the patient’s head as the patient lies back quickly from a sitting to supine position, ending with the head hanging 20 degrees off the end of the examination table (B). The physician turns the patient’s head 90 degrees to the left side. The patient remains in this position for 30 seconds (C). The physician turns the patient’s head an additional 90 degrees to the left while the patient rotates his or her body 90 degrees in the same direction. The patient remains in this position for 30 seconds (D). The patient sits up on the left side of the examination table. (E) The procedure may be repeated on either side until the patient experiences relief of symptoms.

Patients may need to remain upright for 24 hours after canalith repositioning to prevent calcium deposits from returning to the semicircular canals, although this measure is not universally recommended. Contraindications to canalith repositioning procedures include severe carotid stenosis, unstable heart disease, and severe neck disease, such as cervical spondylosis with myelopathy or advanced rheumatoid arthritis.17

Canalith repositioning has been found to be effective in patients with benign paroxysmal positional vertigo. The initial report15 on the Epley maneuver indicated an 80 percent success rate after a single treatment and a 100 percent success rate with repeated treatments. Two subsequent RCTs18,19 reported success rates of 50 to 90 percent. A Cochrane systematic review20 concluded that the Epley maneuver is a safe treatment that is likely to result in improvement of symptoms and conversion from a positive to negative Dix-Hallpike maneuver. However, the review20 noted that no long-term assessment was performed in either RCT18,19 on the use of the Epley maneuver. A study16 of 54 patients with benign paroxysmal positional vertigo found that the modified Epley maneuver was effective in resolving vertigo symptoms after one week of treatment. This study, however, has been criticized for inadequate randomization and lack of blinding of outcome assessors (patient self-report of symptoms).20

One study21 on the long-term effects of canalith repositioning procedures in patients with benign paroxysmal positional vertigo reported a recurrence rate of about 15 percent per year. Another study22 reported recurrence rates of 20 percent at 20 months and 37 percent at 60 months.

VESTIBULAR NEURONITIS AND LABYRINTHITIS

Acute inflammation of the vestibular nerve is a common cause of acute, prolonged vertigo. Associated hearing loss occurs if the labyrinth is involved. The vertigo usually lasts a few days and resolves within several weeks. Many cases of vestibular neuronitis or labyrinthitis are attributed to self-limited viral infections,7 although specific proof of a viral etiology rarely is identified.1

Treatment focuses on symptom relief using vestibular suppressant medications,68 followed by vestibular exercises.14 Vestibular compensation occurs more rapidly and more completely if the patient begins twice-daily vestibular rehabilitation exercises as soon as tolerated after the acute vertigo has been alleviated with medications.7,11

MÉNIÈRE’S DISEASE

Ménière’s disease (or endolymphatic hydrops) presents with vertigo, tinnitus (low tone, roaring, or blowing quality), fluctuating low-frequency sensorineural hearing loss, and a sense of fullness in the ear. In this disorder, impaired endolymphatic filtration and excretion in the inner ear leads to distention of the endolymphatic compartment.

Treatment lowers endolymphatic pressure. Although a low-salt diet (less than 1 to 2 g of salt per day) and diuretics (most commonly the combination of hydrochlorothiazide and triamterene [Dyazide]) often reduce the vertigo, these measures are less effective in treating hearing loss and tinnitus.23,24 Note, however, that the authors of a systematic review25 of treatments for Ménière’s disease criticized the statistical analysis of the frequency of vertigo episodes in one of the studies.23

In rare cases, surgical intervention, such as decompression with an endolymphatic shunt or cochleosacculotomy, may be required when Ménière’s disease is resistant to treatment with diet and diuretics. Ablation of the vestibular hair cells with intratympanic injection of gentamicin also may be effective.26 Surgery usually is reserved for patients with severe, refractory Ménière’s disease.

VASCULAR ISCHEMIA

The sudden onset of vertigo in a patient with additional neurologic symptoms (e.g., diplopia, dysarthria, dysphagia, ataxia, weakness) suggests the presence of vascular ischemia.

Treatment of transient ischemic attack and stroke includes preventing future events through blood pressure control, cholesterol-level lowering, smoking cessation, inhibition of platelet function (e.g., aspirin, clopidogrel [Plavix], aspirin-dipyridamole [Aggrenox]) and, possibly, anticoagulation (warfarin [Coumadin]).

Acute vertigo caused by a cerebellar or brainstem stroke is treated with vestibular suppressant medication and minimal head movement for the first day. As soon as tolerated, medication should be tapered, and vestibular rehabilitation exercises should be initiated.8,10

Placement of vertebrobasilar stents may be considered in a patient with symptomatic critical vertebral artery stenosis that is refractory to medical management.27 Rarely, infarction or hemorrhage in the cerebellum or brainstem may present with acute vertigo as the only neurologic symptom.28 Given the risk of brainstem compression with a large cerebellar stroke, neurosurgical decompression may be indicated.

MIGRAINE HEADACHES

Epidemiologic evidence shows a strong association between vertigo and migraine.29 Diagnostic criteria have been proposed to provide a more specific definition of vertiginous migraine.29 Diagnostic accuracy is important because vertiginous migraine may respond better to migraine treatments than to other interventions.

One retrospective review30 found that migraine treatments were effective in about 90 percent of patients with migraine-associated vertigo. Treatments included dietary changes (i.e., reduction or elimination of aspartame, chocolate, caffeine, or alcohol), lifestyle changes (i.e., exercise, stress reduction, improvements in sleep patterns), vestibular rehabilitation exercises, and medications (e.g., benzodiazepines, tricyclic antidepressants, beta blockers, selective serotonin reuptake inhibitors [SSRIs], calcium channel blockers, antiemetics).

Another retrospective chart review31 demonstrated that stepwise treatment of migraine-associated dizziness (vertigo or dysequilibrium) resulted in complete or dramatic reduction of symptoms in 58 of 81 patients (72 percent). The stepwise treatment consisted of initiating dietary changes, then adding nortriptyline (Pamelor) if needed, then adding atenolol or a calcium channel blocker if needed and, finally, consultation with a neurologist if needed.

A survey32 of 53 patients with migraine at a university-based headache clinic found that the efficacy of medications in treating migraine-associated dizziness was directly correlated with their ability to alleviate migraines. This correlation was strongest in patients with vertigo who were receiving migraine-abortive medications (most significantly, sumatriptan [Imitrex]).

PSYCHIATRIC DISORDERS

Vertigo commonly is associated with anxiety disorders (e.g., panic disorder, generalized anxiety disorder) and, less frequently, depression.33,34 Hyperventilation usually occurs and can result in hypocapnia with reversible cerebral vasoconstriction. Hyperventilation and hypocapnia may be accompanied by dyspnea, chest pain, palpitations, or paresthesias.

Subclinical vestibular dysfunction has been measured in patients with anxiety disorders or depression, most commonly panic disorder with moderate to severe agoraphobia.33 Conversely, classic vertigo resulting from more ostensible vestibular pathology usually induces severe anxiety symptoms and thus can be hard to distinguish from a primary anxiety disorder.

Vestibular suppressants and benzodiazepines most frequently are used to treat dizziness that is associated with anxiety disorder, but these medications provide only transient or inadequate relief.34 SSRIs such as citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft) may provide better relief.

A review34 of 68 patients from a research database at a university neurotology center evaluated open-label SSRI treatment of dizziness associated with psychiatric symptoms (with or without neurotologic illness). Significant improvement of dizziness occurred in 38 patients (63 percent); however, 15 (25 percent) of the 60 patients experienced intolerable side effects. Because some side effects of SSRIs (e.g., nausea, sedation, dizziness) may be more intolerable for patients who have dizziness in association with psychiatric symptoms, slow titration should be used.34

Other medications that are effective in patients with anxiety disorders or depression, such as norepinephrine-serotonin reuptake inhibitors (e.g., venlafaxine [Effexor]) and tricyclic antidepressants (e.g., nortriptyline, desipramine [Norpramin]), have not been evaluated in patients with concomitant vertigo.

Nonpharmacologic treatments for anxiety disorders, such as cognitive behavior therapy, may be helpful. A small prospective RCT of vestibular rehabilitation combined with cognitive behavior therapy to reduce anxiety in older patients with dizziness showed that this combination of treatments improved gait speed and dizziness symptoms but did not improve anxiety or depression.35

PHYSIOLOGIC VERTIGO

Motion sickness9 is attributed to an incongruence in the sensory input from the vestibular, visual, and somato-sensory systems. Motion sickness occurs while riding in a car, boat, or airplane if the vestibular and somato-sensory systems sense movement, but the visual system does not.

On the first sensation of motion sickness, efforts should be made to bring vestibular, visual, and somato-sensory input back in congruence. For example, a person on a boat who starts to feel seasick should immediately watch the horizon. Seasickness can be prevented by applying a scopolamine patch (Transderm-Scop) behind one ear at least four hours before boating.8,36

The Authors

RANDY SWARTZ, M.D., is voluntary associate clinical professor in the Department of Family and Preventive Medicine at the University of California, San Diego, School of Medicine, La Jolla, Calif., and assistant program director at the Scripps Family Practice Residency Program, Chula Vista, Calif. Dr. Swartz graduated from the University of Texas–Houston Medical School and completed residencies in family practice and psychiatry at the Harbor–UCLA (University of California, Los Angeles) Medical Center, Torrance, Calif.

PAXTON LONGWELL, M.D., is a neurologist in private practice in Corpus Christi, Tex. He graduated from the University of Texas–Houston Medical School and completed a residency in neurology at Harbor–UCLA Medical Center.

Address correspondence to Randy Swartz, M.D., 450 Fourth Ave., Suite 201, Chula Vista, CA 91910 (e-mail: swartz.john2@scrippshealth.org). Reprints are not available from the authors.

The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported.

Members of various family medicine departments develop articles for “Practical Therapeutics.” This article is one in a series coordinated by the Department of Family Medicine and Preventive Medicine at the University of California, San Diego, School of Medicine. Guest editor of the series is Tyson Ikeda, M.D.

 

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