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.)