Peripheral vertigo is noted for its abrupt (often explosive)
onset. It is an intense sensation of spinning or hurtling toward
the ground or surrounding walls. It is typically worsened by rapid
movement and by changes in head position. It is frequently associated
with nausea, often severe vomiting, diaphoresis, and bradycardia
BPPV is a mechanical disorder of the inner ear causing transient
vertigo (with autonomic symptoms) and associated nystagmus that
is precipitated by certain head movements.10 The
lifetime prevalence of BPPV is 2.4, with a 1-year incidence of 0.6%.
The mean duration of an episode is 2 weeks; 86% of patients
affected seek medical attention.11
The most widely accepted hypothesis to explain BPPV is known
as canalolithiasis. According to this hypothesis,
BPPV is caused by inappropriate activation of a semicircular canal,
typically the posterior semicircular canal and typically unilateral,
by the presence of free-floating particles or otoconia. The
otoconia become displaced from the utricular macula by aging, head
trauma, or labyrinthine disease. Because the particles are heavier
than the surrounding endolymph, they tend to collect in the long
arm of the posterior semicircular canal, the most dependent part
of the endolymph system. Once the particles clump in sufficient
mass, changes in head position cause gravitation of the particles, which
creates a hydrodynamic drag (or plunger effect) on the endolymph,
causing the cupula to be displaced. This results in inadvertent neural
firing, causing both vertigo and nystagmus.
BPPV can occur at any age, but the average age of onset is in
the mid-50s. Women are twice as likely to be affected as men. The
onset is sudden, and an attack typically is precipitated by rolling
over in bed, assuming a supine position, leaning forward, looking
up at the sky or ceiling, or turning the head. Nausea is often present.
Because the symptoms fatigue, they tend to be worse in the morning
and become less pronounced as the day progresses. Patients may eliminate
the offending activities. There is no associated hearing loss or
tinnitus, and no physical findings on examination of the external
Several findings support a diagnosis of BPPV (Table
164-6). There is a latency period of 1 to 5 seconds between
assuming the offending head position and onset of vertigo and nystagmus.
Both the vertigo and nystagmus crescendo to a peak of intensity
and then subside within 5 to 40 seconds. Posterior canal BPPV
can be diagnosed using the Dix-Hallpike test described above
(see Diagnosis: Physical Examination).11 The response
to repeated provocative testing fatigues, causing the vertigo and nystagmus
to disappear.12 The supine roll test (Pagnini-McClure test13) for horizontal canal BPPV is done as follows:
place the patient supine, turn the head to the right and observe
for nystagmus; then turn head back to neutral position. Repeat,
turning the head to the left. The side of most prominent nystagmus
is the side of the affected canal.
164-6 Supportive Findings in Benign Paroxysmal Positional
Vertigo |Favorite Table|Download (.pdf)
164-6 Supportive Findings in Benign Paroxysmal Positional
|Latency period of <30 s between the provocative head
position and onset of nystagmus.|
|The intensity of nystagmus increases to a peak before slowly
|Duration of vertigo and nystagmus ranges from 5–40
|If nystagmus is produced in one direction by placing the
head down, then the nystagmus reverses direction when the head is
returned to the sitting position.|
|Repeated head positioning causes both the vertigo and accompanying nystagmus
to fatigue and subside.|
BPPV involving the anterior semicircular canal is rare, and the
Dix-Hallpike maneuver may elicit downbeating nystagmus with the
affected ear up. However, any downbeating nystagmus should raise
strong suspicion for a cerebellar or brainstem lesion (Table
164-7 Benign Paroxysmal Positional Vertigo (BPPV) |Favorite Table|Download (.pdf)
164-7 Benign Paroxysmal Positional Vertigo (BPPV)
|Canal Affected by BPPV||Frequency (%)||Diagnostic Maneuver||Nystagmus (direction named by fast component)|
|Posterior||85||Dix-Hallpike, affected ear down||Upbeat, affected ear down|
|Horizontal||10–17||Supine Roll Test (Pagnini-McClure test)||Horizontal, changes direction when head is turned to right
or left while supine|
|Anterior||1||Dix-Hallpike, affected ear up||Downbeating, great concern for brainstem or cerebellar lesions|
The treatment of BPPV includes the use of medications such as
transdermal scopolamine and antihistamines. The particle-repositioning
maneuver (or Epley maneuver; see video: Epley Maneuver) may be attempted by
emergency physicians. The principle behind the particle-repositioning
maneuver is to use gravity to induce the particles to move along
the semicircular canals until they end up inside the utricle, where
they are unlikely to cause vertigo. The maneuver is indicated
in patients who have a history suggestive of BPPV plus a positive
Dix-Hallpike position test with no contraindications to Dix-Hallpike
testing (Figure 164-3).
A through E. Epley Maneuver.
The affected ear is determined by the side on which the Dix-Hallpike
position test is positive. An antihistamine or antiemetic should
be administered before the maneuver for the patient’s comfort.
The patient is seated as in the Dix-Hallpike position test, and
the head is turned 45 degrees toward the affected ear. The patient
is gently brought to the recumbent position with the head hanging
roughly 20 degrees below the examining table. The head is gently
rotated 45 degrees to the midline. The head is then rotated a further
45 degrees to the unaffected side. The patient rolls onto the shoulder
of the unaffected side, at the same time rotating the head a further
45 degrees. The patient is returned to the sitting position, and
the head is returned to the midline. Each portion of the
maneuver should be done slowly (about 5 minutes) and evenly to permit
the particles to traverse their intended course. If the maneuver
is done correctly, nystagmus in the same direction as that observed
during Dix-Hallpike position testing may be observed. If nystagmus
in the opposite direction is observed, then the particles have moved
back toward the cupula; this portends an unsuccessful maneuver. The
maneuver is repeated several times until both the vertigo and the
accompanying nystagmus have disappeared.
The Epley maneuver is a safe and effective treatment for posterior
canal BPPV.13 However, relapses are common.13 Adverse
effects include light-headedness and exacerbation of vertigo (caused
by backsliding of the particles). The Epley maneuver should not
be performed on patients with the same conditions as described above
for the Dix-Hallpike maneuver.
Most episodes of BPPV resolve spontaneously after a few days.
Patients with persistent symptoms should be referred to an otolaryngologist.
Ménière disease is a disorder associated with
an increased endolymph within the cochlea and labyrinth. It occurs
equally in men and women. The first attack of Ménière
disease usually occurs in patients aged 65 years and older, but
may rarely begin in childhood. The disease is usually unilateral
but may become bilateral over time. The precise pathogenesis is
unknown, but evidence suggests that patients have difficulty regulating
the volume, flow, and composition of endolymph. As with BPPV, the onset
of vertigo is usually sudden, with associated nausea, vomiting,
and diaphoresis. The duration of vertigo ranges from 20 minutes
to 12 hours (typically, 2 to 8 hours). The frequency of attacks
varies from several times per week to several times per month. Other
associated symptoms include roaring tinnitus, diminished hearing,
and fullness in one ear. Between attacks, the patient is usually
well, although decreased hearing may persist. The diagnosis
of Ménière disease is confirmed by glycerol testing
and by vestibular-evoked myogenic potentials.14
Patients with Ménière disease usually are referred
to an otolaryngologist for a variety of treatment options. Ménière
disease may be managed symptomatically with antihistamines, betahistine,
and calcium channel blockers, as well as with a combination of the
diuretics triamterene and hydrochlorothiazide (the latter two drugs
are used in confirmed cases only). Betahistine has been shown to
be superior to calcium channel blockers in patients with Ménière
disease. Calcium channel blockers such as flunarizine (not available
in the U.S. at the time of this writing), are considered options
in the management of vertigo associated with Ménière
disease (Table 164-5). None of these drug
treatments improves hearing. A salt-restricted diet (<1 gram/d
of added salt) is recommended for patients with a confirmed diagnosis.
Intratympanic gentamicin administration (usually be an otolaryngologist)
has been shown to provide significant immediate and long-term relief
in patients with Ménière disease.15
A perilymph fistula is an opening in the round or oval window
that permits pneumatic changes in the middle ear to be transmitted
to the vestibular apparatus. Trauma, infection, or a sudden change
in the pressure inside the ventricular system may cause the tear.
The diagnosis is suggested by the sudden onset of vertigo associated
with flying, scuba diving, severe straining, heavy lifting, coughing,
or sneezing. Associated symptoms may include hearing loss. The
diagnosis is confirmed by nystagmus elicited by pneumatic
otoscopy (Hennebert sign). Hearing
loss is confirmed by audiology testing.
Perilymph fistula is managed with symptomatic treatment and bed
rest, with referral to an ENT specialist for surgical repair. Fistulas
associated with hearing loss of <14 days’ duration may
benefit from rapid surgical intervention.
Vestibular neuronitis is a disorder of suspected viral etiology.
Unlike BPPV and Ménière disease, vestibular neuronitis
typically lasts several days and does not recur. The onset is usually
sudden, and the patient is otherwise well except for possible symptoms
of a viral illness. The vertigo is often so intense that the patient
requires several days of bed rest; symptoms usually decrease dramatically,
with complete resolution over several weeks. Elderly patients may
have persistent unsteadiness of gait. Unilateral loss of hearing
and tinnitus may occur. Up to one third of patients have positional
nystagmus. Vestibular neuronitis is treated symptomatically.
Vestibular ganglionitis is believed to be caused by a neurotrophic
virus such as varicella zoster that can be reactivated years following
an initial infection. Typical histopathologic changes associated
with a viral inflammatory process have been identified in the vestibular
ganglion. This disorder may be mistaken for BPPV and Ménière
disease. Multiple ganglia may be involved. Herpes zoster oticus,
also known as the Ramsay Hunt syndrome,
is a neuropathic disorder thought to be associated with vestibular
ganglionitis. It is characterized by deafness, vertigo, and
facial nerve palsy. The diagnosis is confirmed by the presence
of grouped vesicles on an erythematous base inside the external
auditory canal. Patients with this disorder are managed with
a combination of symptomatic treatment and antiviral therapy started
within 72 hours of the appearance of vesicles.
Labyrinthitis is an infection of the labyrinth that produces
peripheral vertigo associated with hearing loss. The infection may
be viral (associated with measles and mumps), in which case the
clinical course is similar to that of vestibular neuronitis. Bacteria
also may cause labyrinthitis as a sequela of otitis media, in which
bacteria and toxins diffuse across the membrane of the round window.
A cholesteatoma can erode into the inner ear, creating a portal
of entry for bacteria. Other possible antecedents for bacterial
labyrinthitis include otitis media with fistula, meningitis, mastoiditis,
and dermoid tumor. The hallmarks of this disease include sudden
onset of vertigo with associated hearing loss and middle ear findings. Serous
labyrinthitis occasionally may produce vertigo.
Patients with bacterial labyrinthitis are at risk for meningitis
and require antibiotics and referral to an otologist or ENT specialist
for admission and possible surgical drainage.
Ototoxicity has been associated with aminoglycoside
and macrolide antibiotics, loop diuretics, platinum-based chemotherapeutic
agents, some NSAIDs, and antimalarial preparations.16 Aminoglycoside antibiotics produce
hearing loss and peripheral vestibular dysfunction by accumulating
inside the endolymph, where they cause the death of cochlear and vestibular
hair cells. However, because both inner ears are affected, vertigo
is uncommon. Its clinical manifestations include ataxia and oscillopsia,
which is defined as an inability to maintain visual fixation while moving.
The damage is usually irreversible but is dose- and duration-dependent.
Loop diuretics (furosemide and ethacrynic acid) also cause irreversible
vestibular and ototoxicity. It has recently been suggested that N-acetylcysteine
administered orally may help prevent aminoglycoside-induced ototoxicity in
hemodialysis patients.17 Cytotoxic agents associated
with vestibular damage include vinblastine and cisplatin. The topical
administration of d-methionine to the round window
membrane may protect against the ototoxic effects of cisplatin.
Newer platins, such as carboplatin, have been shown to induce less
ototoxicity than cisplatin. The antiarrhythmic drug quinidine and
antimalarial drugs derived from quinine, such as chloroquine and
mefloquine, also can cause vestibular symptoms that may be irreversible
Table 164-8 Ototoxic and
Vestibulotoxic Agents |Favorite Table|Download (.pdf)
Table 164-8 Ototoxic and
|Aminoglycosides||Yes||Usually not; possible improvement with N-acetylcysteine|
|Loop diuretics||No||Can be irreversible|
Reversible causes of vestibular damage and ototoxicity include
NSAIDs, salicylates, minocycline, erythromycin, and some fluoroquinolones.
Salicylate ingestion may be associated with tinnitus as well as
altered perception of sounds. Rarely, sudden hearing loss has been
associated with other NSAIDs, including ketorolac, naproxen, and
piroxicam (the latter two associated with tinnitus).17,18 Isolated
cases of unsteady gait have been observed with antiviral drugs such
as abacavir as well as antiparasitic agents.
Numerous solvents and other chemicals can cause both peripheral
and central vestibular symptoms. These include propylene glycol,
toluene, mercury, and hydrocarbons. Drugs that sometimes induce a central vestibular
syndrome include anticonvulsants, tricyclic antidepressants, neuroleptics,
opiates, and alcohol.19 Phencyclidine is a recreational
drug that causes central vestibular symptoms, including nystagmus
and ataxia. Drugs causing irreversible cerebellar toxicity include
phenytoin and toluene, as well as cancer chemotherapeutic agents.
In general, most patients adapt to vertigo that is chronic by relying
on increased sensory input from unaffected modalities such as proprioception
and vision. However, certain drugs that are used as antivertigo
therapy may exacerbate preexisting chronic vertigo by delaying or
inhibiting such compensation. These drugs include alcohol, benzodiazepines,
barbiturates, and neuroleptics. Thus, with chronic vertigo, antivertigo
therapy should not be used on a long-term basis. Patients with suspected
ototoxicity should be referred to an otolaryngologist.
Lesions of the eighth cranial nerve may produce mild vertigo. Meningiomas and acoustic
schwannomas are typical causes. The onset of vertigo is usually
gradual, remaining constant until central compensation can take
place. The vertigo is usually preceded by hearing loss. Such patients require
urgent diagnostic imaging as well as referral to a neurosurgeon.
Vertigo is sometimes associated with tumors of the cerebellopontine
angle. Such tumors include acoustic neuromas, meningiomas, and dermoids. They
usually present with a cluster of findings, including deafness and ataxia,
as well as ipsilateral facial weakness, loss of the corneal reflex, and
cerebellar signs. Such patients require urgent diagnostic
imaging as well as referral to a neurosurgeon.
Vertigo and gait unsteadiness are common complaints following
a head injury. Acute post-traumatic vertigo is caused by a direct
injury to the labyrinthine membranes. The onset of vertigo is immediate
and is accompanied by nausea and vomiting. Such patients may have
sustained a concomitant fracture of the temporal bone. Vertigo associated
with a closed head injury warrants a CT scan or MRI to exclude an
extradural or intradural hematoma. Vertigo due to direct labyrinthine
trauma tends to resolve within several weeks. Closed head trauma
also can displace otoconia from the utricular maculae, precipitating
an attack of BPPV. Postconcussive syndrome can be associated with
unsteadiness of gait and a vague sense of dizziness. Patients with
this condition may be treated symptomatically, with referral to
a specialist for patients whose symptoms fail to resolve.
Vertigo after Cochlear
Vertigo is a well-known complication of cochlear implantation.
The etiology is likely multifactorial and includes the dislodging
of otoconia and the introduction of bone dust into the labyrinth.20