General

Vertigo is diagnosed in roughly half of patients reporting dizziness. It is defined as the sensation of movement when none exists. About 80% of cases of vertigo are due to a peripheral lesion (pathology of the vestibular structures or cranial nerve VIII). Although peripheral vertigo is benign and not life-threatening, it may cause significant disability.

Benign Paroxysmal Positional Vertigo

The most common type of vertigo is benign paroxysmal positional vertigo (BPPV).¹ It occurs in all age groups but becomes more common with aging. Women are affected twice as often as men.

Vestibular Neuritis and Labyrinthitis

These disorders most commonly occur in patients in the third to fifth decades of life. Peripheral vestibulopathies typically follow viral gastrointestinal or upper respiratory infections.

Benign Paroxysmal Positional Vertigo

BPPV results from a mechanical defect in the inner ear. Canalolithiasis is the most accepted hypothesis. According to this premise, the culprits are free-floating otoliths that have become displaced from the utricle and inappropriately enter and activate the end-organs of the semicircular canals.² With certain head movements, a clump of otoliths moves, causes the endolymph to move with resultant inappropriate displacement of the cupula. Movement of the cupula triggers neural firing, with consequential vertigo and nystagmus. Less commonly, otoliths can adhere to the cupula and result in vertigo. This mechanism is called cupulolithiasis.

Although any semicircular canal can be affected, the posterior (inferior) canal is involved approximately 95% of the time because the otoliths, when displaced from the utricle, fall into the most dependent part of the system—the long arm of the posterior semicircular canal. BPPV is generally unilateral.

Vestibular Neuritis and Labyrinthitis

Sometimes referred to as vestibular neuronitis, vestibular neuritis occurs as a result of viral inflammation of the vestibular nerve. Unlike labyrinthitis, no auditory symptoms are present.

Labyrinthitis is caused by an infectious inflammation of the labyrinth. Viral causes are most common, although labyrinthitis may also occur as a result of Lyme neuroborreliosis or otosyphilis infections. Disruption of the round window by otitis media or cholesteatoma gives pathogens access to the labyrinth. Tumors, fistulas, meningitis, or mastoiditis may also create a portal of entry. Unilateral hearing loss and tinnitus are the distinguishing factors of labyrinthitis.

See Table 96.2 for the pathophysiology of other causes of peripheral vertigo.

Table 96.2 Pathophysiology of Various Causes of Peripheral Vertigo

BPPV, Benign paroxysmal positional vertigo; VN/L, vestibular neuritis/labyrinthitis.

Benign Paroxysmal Positional Vertigo

In BPPV, sudden transient vertigo is brought on by a change in head position. After head movement there is a delay of a few seconds, and then the room starts to spin and the patient experiences nausea or vomiting, or both. If the head is kept motionless, these symptoms typically resolve within 10 to 30 seconds. The symptoms are generally worse in the morning, probably because the otoliths have clumped together during sleep and exert a greater mass effect when the patient rolls over on awakening in the morning. The vertigo will tend to lessen as the day goes on because the otoliths become more dispersed and exert less of a mass effect.

The diagnosis of BPPV is confirmed with the Dix-Hallpike test,³ also called the Nylan-Bárány test (Fig. 96.1; Box 96.2).

Fig. 96.1 The Dix-Hallpike test of a patient with benign paroxysmal positional vertigo affecting the right ear.

In A, the examiner stands at the patient’s right side and rotates the patient’s head 45 degrees to the right to align the right posterior semicircular canal with the sagittal plane of the body. In B, the examiner moves the patient, whose eyes are open, from the seated to the supine right ear–down position with the head extended past the edge of the examination table. The latency, duration, and direction of nystagmus, if present, and the latency and duration of vertigo, if present, should be noted. The arrows in the inset depict the direction of nystagmus in patients with typical benign paroxysmal positional vertigo. The presumed location in the labyrinth of the free-floating otoliths thought to cause the disorder is also shown.

(From Furman JM, Cass SP. Benign paroxysmal positional vertigo. N Engl J Med 1999;341:1590–6.)

The patient should sit on one end of the examination table so that the head hangs over the edge when lying down. Because visualization of the direction of nystagmus is important, the patient should be instructed to keep the eyes open during the test. The purpose of the Dix-Hallpike test is to determine whether otoliths are inappropriately placed in the posterior semicircular canal. Thus the goal is to try to move potential otoliths that are located in the posterior semicircular canal, which will elicit symptoms and nystagmus. The most provocative way to get otoliths to move is to first align the posterior canal in the same plane as the upcoming movement (lying supine). This is why the patient’s head, while sitting up, is first turned 45 degrees to the side being tested. The patient then lies back down so that the head overhangs the edge of the examination table. A positive test results in transient reproduction of the patient’s symptoms and transient torsional nystagmus in which the fast phase is upbeat (toward the forehead). The patient then sits up and the test is repeated with the head rotated 45 degrees to the opposite side. In general, the test should be positive with the head turned only to one side, and this becomes the starting side for the potentially curative Epley maneuver (to be discussed later).

Occasionally, the horizontal semicircular canal is affected, and this is diagnosed with the roll test. The patient lies supine (unlike the Hallpike test, the head does not need to extend off the edge of the examination table). The head is then turned to each side approximately 90 degrees. Reproduction of the symptoms and nystagmus should occur, with the fast phase of the nystagmus beating downward toward the dependent ear. The side that is involved is the one that has the more acute symptoms and more severe nystagmus.

Vestibular Neuritis and Labyrinthitis

Spontaneous vertigo develops over a period of hours. Nausea and vomiting may occur. Symptoms that accompany a viral illness may also be present. The vertigo is initially severe, may require 1 or 2 days of bed rest, and then gradually resolves over a few weeks.

Spontaneous nystagmus with peripheral features may be seen on examination. Postural imbalance with a tendency to fall toward the side with the lesion is also seen. Middle ear infection or serous fluid may be present. Patients have a positive head-thrust test,⁴ also known as the head impulse test.

The head-thrust test begins by directing the patient to look straight ahead. The examiner then places both hands on the patient’s head and rapidly thrusts the patient’s head to one side approximately 10 degrees. Normally, the patient’s eyes will remain focused straight ahead when the head is turned rapidly. In patients with unilateral peripheral vestibular loss, such as occurs with vestibular neuritis and labyrinthitis, the eyes will move with the head but then a corrective saccade will bring the eyes back to the midline. Visualization of a corrective saccade (a positive test) confirms the diagnosis. Both sides should be tested.

Computed Tomography

Because skull-related artifacts are common with computed tomography, it has limited utility for evaluating the posterior fossa. If a patient has a focal neurologic finding and normal results on computed tomography, further imaging is necessary.

Magnetic Resonance Imaging and Magnetic Resonance Angiography

For assessment of pathologic causes of vertigo, magnetic resonance imaging (MRI) is the modality of choice. Magnetic resonance angiography is a noninvasive technique that can be used to visualize the vessels of the posterior circulation. It can detect aneurysms, atherosclerosis, dissections, vasculitis, thrombosis, and other processes.

Laboratory Testing

Laboratory testing is rarely useful in the initial evaluation of a vertiginous patient. Screening tests include hematocrit, glucose, and electrolyte levels.

Electrocardiography

An electrocardiogram is useful to evaluate for signs of cardiac ischemia or dysrhythmia.

Benign Paroxysmal Positional Vertigo

The Epley maneuver takes approximately 3 minutes and has been shown to be safe and effective in treating posterior canal BPPV.⁶ It is also easily performed in the ED setting. Gravity is used to move the otoliths out of the posterior semicircular canal into the utricle, where they will no longer cause vertigo.

The starting position of the Epley maneuver is determined by the diagnostic Hallpike test (recall that only one side should be positive). As in the Hallpike test, the patient sits upright with the head turned 45 degrees to the affected side and then lies down with the head overhanging the edge of the examination table. This maneuver should cause reproduction of the symptoms and torsional nystagmus.

Next, the head is rotated 90 degrees to the opposite side while it remains overhanging the edge of the examination table. The patient now rolls over onto the side and turns the head toward the ground. The patient is instructed to not lift the head up while turning onto the side. The patient is then brought up to the sitting position (the legs can hang over the side of the examination table or return to the original starting position), and the head is brought forward slightly.

Each position is held for approximately 30 seconds or until the symptoms and nystagmus resolve. It is currently recommended that the patient remain upright at least 20 minutes after the maneuver, which may be sufficient time for the otoliths to reattach to hair cells in the utricle (Fig. 96.2).

Fig. 96.2 Epley maneuver.

(Adapted from Timothy C. Hain, MD. Available at http://www.dizziness-and-balance.com/disorders/bppv/bppv.html.)

The Semont liberatory maneuver can also be used to treat BPPV. The patient sits upright in the middle of the examining table with his legs overhanging the edge of the gurney. The head is turned 45 degrees to the side opposite the involved canal. The patient is then rapidly laid down sideways to the side opposite of the direction his head is turned. Then the patient is rapidly laid down sideways to the other side, such that the patient’s face is now directed toward the gurney. The patient then returns to the sitting position. The author does not recommend the use of this maneuver because the rapid movements are not likely to be tolerated, especially by elderly patients.

Patients with a positive roll test (indicating horizontal semicircular canal involvement) can be treated with the barbeque roll maneuver in which the patient is placed in the supine position with the head turned 90 degrees to the affected side as determined by the roll test. The head is then turned in 90-degree intervals in the opposite direction back to the original starting position. This requires the patient to eventually turn onto the abdomen. Each position is held for 30 seconds or until resolution of the vertigo and nystagmus. Anterior canal BPPV is diagnosed by a characteristic history, as well as by downbeat torsional nystagmus during the Dix-Hallpike test. Because downbeat (fast phase beating toward the feet) nystagmus can also indicate a central cause of vertigo and anterior canal involvement is extremely rare,⁷ the author cautions against making this diagnosis and recommends consideration of a central cause of vertigo.

Vestibular Neuritis and Labyrinthitis

A recent multicenter trial sought to treat vestibular neuritis in a manner similar to Bell palsy. The study found that a 22-day taper of methylprednisolone was beneficial but that valacyclovir was not.⁸

Benign Paroxysmal Positional Vertigo

BPPV is generally self-limited but recurs up to 50% of the time.⁷ Persistent or recurrent vertigo is managed with the maneuvers described previously. Vestibular suppressants may also be prescribed.

Patients who work at heights (builders, roofers) should curtail activities until their symptoms have resolved. All patients can benefit from specialist referral. Outpatient contrast-enhanced MRI may be used to look for an acoustic neuroma or other pathology that can mimic BPPV.

In some intractable incapacitating cases, patients may benefit from neurectomy or nonampullary plugging of the semicircular canal.⁹

Migraine

The lifetime prevalence of migraine (16%) and vertigo (7%) leads to an expected comorbidity of the two conditions in 1.1% of the general population.¹⁰ A recent German survey, however, found a prevalence of 3.2%.¹¹ Vestibular migraines are the most common cause of central vertigo and occur in 25% of patients suffering from migraines. Vestibular migraines tend to occur in women between the third and fifth decades of life.

Stroke

Each year 795,000 people suffer a new or repeated stroke, and stroke remains the third leading cause of death in the United States. Twenty percent of strokes involve the posterior circulation, which can affect the vestibular structures or pathways leading to vertigo.

Migraine

It has been theorized that the increased sensitivity to vestibular input in patients with vestibular migraine is analogous to the increased sensitivity causing photophobia and phonophobia in patients with typical migraines.

Stroke

The CNS obtains its blood supply from the carotid and vertebral arteries. The carotid arteries are referred to as the anterior circulation and the vertebral arteries as the posterior circulation. These two arterial systems join at the base of the brain in the vascular circle of Willis. Smaller arteries branch off from this anastomosis to supply specific areas of the brain. Blockage of one of these arteries results in a recognizable pattern of signs and symptoms consistent with the brain territory affected. A stroke is caused by thrombosis, hemorrhage, or embolism in one of the cerebral arteries. Vertigo secondary to stroke generally indicates involvement of the posterior circulation.

Other

The pathophysiology of selected other causes of central vertigo are listed in Box 96.4.

Migraine

If a preceding aura occurs, the migraine will usually develop over a period of minutes and subside within an hour. This is followed by the acute onset of vertigo. Patients usually have an associated headache; however, vertigo may be the headache equivalent.¹² Fluctuating low-frequency hearing loss and tinnitus can also occur (Box 96.5).

Stroke

Twenty percent of strokes involve the posterior circulation, which can affect the vestibular structures or pathways leading to vertigo. Symptoms of stroke vary depending on the affected anatomy and vasculature but often involve one or more of the “five D’s”: dizziness, diplopia, dysarthria, dysphagia, and dystaxia. The vascular structures most commonly affected by stroke and other lesions can be divided into anatomic territories, including the vertebrobasilar territory, the superior cerebellar artery territory, and the posterior inferior cerebellar artery territory (see Table 96.5).

The hallmark of many brainstem strokes is crossed signs (e.g., contralateral sensory and motor findings). Vertigo and nystagmus occur early in the progression of ischemia. Dysarthria and oculomotor deficits develop later in the course and portend major neurologic catastrophe.

Migraine

MRI may be performed to evaluate for a cerebellar or brainstem lesion if suspected.

Stroke

Although computed tomography may show large bleeding, MRI is best for imaging the posterior fossa.

Acute posterior circulation infarcts are best seen on diffusion-weighted MRI. Magnetic resonance angiography is used to additionally assess the vertebral arteries. Patients with contraindications to MRI should undergo computed tomography and computed tomographic angiography. Carotid ultrasound scanning is not helpful in patients with posterior ischemia. Electrocardiography, echocardiography, and rhythm monitoring are important in evaluating cardiac and aortic sources of embolism.

Migraine

Information on specific treatment of vertiginous migraines is limited (e.g., patients should avoid migraine triggers) and is not based on controlled studies. Patients should be referred to a neurologist for follow-up.

Stroke

Although intravenous tissue plasminogen activator (t-PA) may enhance recovery if given within 3 hours of the onset of ischemic stroke, mixed results are found when t-PA is used for vertebrobasilar disease.¹³

Other

Ventriculostomy and occipital craniotomy are often performed to relieve pressure within the posterior fossa associated with hemorrhage or a mass effect. Administration of mannitol should be considered for patients with signs of herniation.

Hypotension should be corrected because it worsens symptoms and outcome. Intravenous fluids, blood, and pressors should be administered as needed. Neurologic consultation may be useful to guide treatment.