Evaluation of The Patient With Vertigo

Evaluation of the patient with vertigo - UpToDate 5/03/18, 11)27 p. m.
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Evaluation of the patient with vertigo
Authors: Joseph M Furman, MD, PhD, Jason JS Barton, MD, PhD, FRCPC
Section Editors: Michael J Aminoff, MD, DSc, Robert S Hockberger, MD, FACEP, Daniel G Deschler, MD, FACS
Deputy Editor: Janet L Wilterdink, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2018. | This topic last updated: Jun 10, 2015.
INTRODUCTION — Vertigo is a symptom of illusory movement. Almost everyone has experienced vertigo as the
transient spinning dizziness immediately after turning around rapidly several times. Vertigo can also be a sense
of swaying or tilting. Some perceive self-motion whereas others perceive motion of the environment.
Vertigo is a symptom, not a diagnosis. It arises because of asymmetry in the vestibular system due to damage to
or dysfunction of the labyrinth, vestibular nerve, or central vestibular structures in the brainstem.
Vertigo is a troubling problem for many clinicians because it is symptomatic of a large range of diagnoses from
benign to immediately life threatening (table 1). However, in most cases, the clinical history, especially the tempo
of the symptoms (table 2), with examination findings that distinguish between central and peripheral etiologies
(table 3) identify those patients that require urgent diagnostic evaluation.
Vertigo is only one type of dizziness. Other symptoms that patients may identify as dizziness include presyncopal
faintness, disequilibrium, and nonspecific or ill-defined light-headedness. The initial approach to the patient who
complains of dizziness is to localize the cause of the symptom into one of these broad categories. This is
described separately. (See "Approach to the patient with dizziness".)
This topic will discuss the clinical approach to a patient with vertigo. The pathophysiology, etiology, and treatment
of vertigo are discussed separately. (See "Pathophysiology, etiology, and differential diagnosis of vertigo" and
"Treatment of vertigo".)
CLINICAL FEATURES
Vertigo — Vertigo is the predominant symptom of vestibular dysfunction. Patients often experience vertigo as an
illusion of motion; some interpret this as self-motion, others as motion of the environment. The most common
motion illusion is a spinning sensation. A spinning sensation is not required; vertigo can also be a sense of
swaying or tilting. Also, not all patients are able to describe their vertigo in such concrete terms. Vague dizziness,
imbalance, or disorientation may eventually prove to be due to a vestibular problem [1]. On the other hand, some
patients with presyncope sometimes interpret the woozy, faint feeling as a spinning sensation. Thus, a symptom
of vertigo is not a perfectly sensitive or specific for a vestibular problem.
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Severe vertigo may occur with both acute central and peripheral lesions. However, when symptoms are less
pronounced, particularly when there is pronounced nystagmus out of proportion to the severity of vertigo, this
strongly suggests a brainstem rather than a peripheral lesion.
Nausea and vomiting — Nausea and vomiting are typical with acute vertigo, unless it is mild or very brief, as
with benign paroxysmal positional vertigo. Vomiting can be severe, causing dehydration and electrolyte
imbalance. Severe nausea and vomiting are more common with peripheral than central lesions but can occur
with both [2].
Postural and gait instability — Postural stability can be affected in patients with vertigo. The vestibular nuclei
send signals to the vestibulospinal tract, which in turn stimulates antigravity muscles that maintain posture.
The effects of unilateral lesions of the vestibular apparatus upon postural stability are variable. In general, vertigo
of central origin impairs gait and posture to a greater degree than does vertigo of peripheral origin, probably
because central etiologies likely also impair other pathways involved in balance and posture [1,2]. Patients with
vertigo of peripheral origin are usually able to walk, but may be very reluctant to move.
Other symptoms of vestibular dysfunction — Patients with vestibular injury may not complain of vertigo. In
fact, vertigo is unusual in chronic vestibular injury or acute, bilaterally symmetric vestibular injury. Other
symptoms of vestibular injury may include:
Tilt illusion — A tilt illusion in which patients feel that they and their environment are tilted with respect to
gravity, even to the point of being upside down, usually reflects damage to otolithic organs (utricle and saccule)
or their central connections. Otolith dysfunction may also cause lateropulsion or the tendency to fall to the side of
the lesion.
Drop attacks — Patients with drop attacks of vestibular origin often have a sensation of being pushed or
pulled to the ground [3,4]. Unlike presyncope and seizures, there is no faintness or loss of consciousness with
drop attacks.
Drop attacks are often attributed to a sudden loss of tone mediated by vestibulospinal reflexes, but can have
other causes as well. (See "Seizures and epilepsy in older adults: Etiology, clinical presentation, and diagnosis",
section on 'Drop attacks'.)
Drop attacks are an unusual feature of Meniere disease. Sometimes called Tumarkins' otolithic crises, this
symptom is usually seen only in advanced cases. Superior canal dehiscence and aminoglycoside toxicity are
also associated with this presentation [5,6].
Spatial disorientation — A fleeting spatial disorientation with rapid head turns often remains after the patient
has recovered from an acute attack of vertigo. The most astute patients will observe that this is more pronounced
with head turns to the side of the lesion.
Oscillopsia — Oscillopsia, a visual illusion of to-and-fro environmental motion, and blurred vision whenever
the head is in motion is a manifestation of an impaired vestibuloocular reflex. Affected patients notice that
everything jiggles when they are walking or driving on rough pavement; they often have to stop and stand still to
read signs.
Impaired balance without vertigo — This is a common manifestation of acute simultaneous bilateral
vestibular loss such as that occurring with aminoglycoside antibiotic toxicity. Vertigo does not occur because
there is no marked vestibular asymmetry. Most patients have oscillopsia during passive head movement, as
when walking or riding in a car over rough terrain [7]. Imbalance is most marked in the dark when visual cues to
position in space are not available. Aminoglycoside toxicity is the most common identified etiology of bilateral
vestibulopathy, followed by Meniere disease and meningitis [8]. Bilateral vestibular failure is also a key feature of
CANVAS (cerebellar ataxia, neuropathy and vestibular areflexia syndrome) [9]. Most cases, however, are
cryptogenic in origin. This presentation is also characteristic of acute midline cerebellar lesions or thiamine
deficiency. (See "Wernicke encephalopathy" and "Overview of cerebellar ataxia in adults", section on 'Autosomal
recessive ataxias'.)
EVALUATION
History — The history should allow the clinician to distinguish vertigo from other types of dizziness and to make
a hypothesis about the site and type of lesion. It is customary to organize causes of vertigo into peripheral and
central disorders (table 1). These have distinctive clinical features, but with some overlap. The clinical features of
the most common disorders are summarized in the Table (table 2).
Time course — Vertigo is never a permanent, continuous symptom. Even when the vestibular lesion is
permanent, the central nervous system adapts to the defect so that vertigo subsides over days or weeks.
Constant dizziness lasting months is not vestibular. However, some patients describe constant dizziness but
actually mean that they have a constant susceptibility to frequent episodic dizziness.
Vertigo can occur as single or recurrent episodes and may last seconds, hours, or days. This time course of
symptoms provides one of the best clues to the underlying pathophysiology of vertigo (table 2).
● Recurrent vertigo lasting under one minute is usually benign paroxysmal positional vertigo [10].
● A single episode of vertigo lasting several minutes to hours may be due to migraine or to transient ischemia
of the labyrinth or brainstem [11].
● The recurrent episodes of vertigo associated with Meniere disease or recurrent vestibulopathy also typically
last hours but can be briefer [12,13].
● More prolonged, severe episodes of vertigo that occur with vestibular neuritis can last for days [14,15]. This
is also characteristic for vertigo originating from multiple sclerosis or infarction of the brainstem or
cerebellum.
Aggravating and provoking factors — All vertigo is made worse by moving the head. Many patients in the
midst of a vertiginous attack may be petrified to move. If head motion does not worsen the feeling, it is probably
another type of dizziness. This feature does not distinguish causes of vertigo [16].
Attacks of benign paroxysmal positional vertigo are often provoked with specific head movements or postures
(eg, rolling over in bed, extending the neck).
Vertigo aggravated by coughing, sneezing, exertion, or loud noises (Tullio phenomenon) should raise suspicion
of either a perilymphatic fistula, in which there is an abnormal connection between the middle ear and the
perilymphatic space of the inner ear, or a superior canal dehiscence, in which there is a defect in the roof of the
superior canal. Both conditions allow pressure to be transmitted from the cerebrospinal fluid (CSF) space to the
inner ear [17,18]. (See "Pathophysiology, etiology, and differential diagnosis of vertigo".)
Head trauma is an important historical feature and can produce vertigo by a variety of mechanisms [19]. (See
"Acute mild traumatic brain injury (concussion) in adults".) Barotrauma, middle ear surgery, and straining with
weight lifting and bowel movements have also been reported to produce a perilymphatic fistula.
Recent hyperextension injury to the neck, usually with persistent neck pain, suggests the possibility of vertebral
artery dissection with brainstem or labyrinthine ischemia.
Recent viral symptoms may suggest acute vestibular neuritis, which is believed to be produced by viral or
postviral inflammation of the eighth cranial nerve. However, a history of recent viral illness is both nonspecific
and insensitive; less than one-half of patients with vestibular neuritis will report this [14,20,21].
Associated symptoms — A number of associated symptoms may help to distinguish the etiology of vertigo:
● Acute vertigo due to a vertebrobasilar stroke is almost always accompanied by other evidence of brainstem
ischemia such as diplopia, dysarthria, dysphagia, weakness, or numbness [1]. However, infarction of the
cerebellum may present as vertigo with no other symptoms. Focal neck pain may suggest vertebral artery
dissection.
● Vertigo in patients with multiple sclerosis may also be preceded by or associated with other neurologic
dysfunction depending on the locus of demyelination.
● Deafness and tinnitus suggest a peripheral lesion of the inner ear. A sensation of aural fullness typically
accompanies attacks of Meniere disease [13]. (See "Meniere disease".) A pressure sensation in the ear and
high frequency sensorineural hearing loss can be associated with the development of a traumatic
perilymphatic fistula [19].
● Headache, photophobia, and sonophobia suggest migrainous vertigo. Most patients with migrainous vertigo
will also experience visual aura in at least some of their attacks.
● Shortness of breath, palpitations, and sweating may suggest a panic attack, but true vertigo is often so
terrifying that such symptoms are not uncommon with vestibular disease [22].
Prior medical history
● A prior history of migraine suggests that this may be the etiology of vertigo.
● The presence of stroke risk factors such as hypertension, diabetes mellitus, smoking, and a history of
vascular disease support a diagnosis of vertebrobasilar ischemia [1]. Patients with an episode of vertigo and
one or more risk factors have a substantial risk of subsequent stroke: an 8 percent 2-year risk with one or
two risk factors and 14 percent 2-year risk with three or more risk factors [23].
● Past head trauma is a common antecedent to benign paroxysmal positional vertigo. Less commonly, head
trauma or barotrauma can cause a perilymphatic fistula.
● A family history of vertigo may suggest a rare hereditary channelopathy.
● Certain medications are associated with vestibular (eg, cisplatin, aminoglycosides) or cerebellar (eg,
phenytoin) toxicity.
Examination — The physical examination should confirm vestibular dysfunction and distinguish central from
peripheral causes of vertigo. Features most helpful in distinguishing central and peripheral vertigo are shown in
the Table (table 3).
Nystagmus — Nystagmus is a rhythmic oscillation of the eyes. There are many types of nystagmus. Some
types of nystagmus suggest that a patient's complaint of vertigo originates from pathology in the vestibular
system.
An important role of the vestibular system is to maintain gaze during head movement through the vestibular
ocular reflexes. Acute unilateral vestibular lesions lead to a pathologic asymmetry in vestibular activity. This
results in a slow drift of the eyes away from the target in one direction, followed by a fast corrective movement in
the reverse direction. The eyes appear to "beat" in the direction of the fast phase. This nystagmus, which is often
labeled “spontaneous nystagmus”, continues until the asymmetry of vestibular activity is restored to normal or
until the central nervous system adapts to the vestibular lesion. (See "Overview of nystagmus".)
In a patient with acute vertigo, nystagmus is usually visible with the patient looking straight ahead. If the lesion is
peripheral, the fast phase is away from the affected side. Usually, nystagmus increases in frequency and
amplitude with gaze toward the side of the fast phase, eg, leftward gaze increases left-beating nystagmus, if
present.
Other features of the nystagmus have localizing value for central versus peripheral vertigo (table 3):
● Type of nystagmus. A mixed horizontal-torsional nystagmus results if a peripheral lesion affects all three
semicircular canals on one side. The horizontal fast phases beat toward the normal ear, as do the upper
poles of the eyes for the torsional fast phases. The nystagmus from peripheral disease occasionally appears
purely horizontal, but it is never purely torsional or vertical. The nystagmus with central lesions may have
any trajectory.
● Visual fixation tends to suppress nystagmus that is due to a peripheral lesion, but it does not usually
suppress nystagmus from a central lesion [24]. It may be useful to inhibit visual fixation to test whether the
nystagmus is central or peripheral in origin. Frenzel lenses are large magnifiers that blur vision and prevent
visual fixation. A peripheral lesion is likely if nystagmus increases when Frenzel lenses are in place. The
effect of fixation can also be determined during ophthalmoscopy if the examiner covers and uncovers the
other eye. One group of investigators has proposed that examination with a penlight (substituting for the
ophthalmoscope) may also allow examination for nystagmus with and without fixation [25]. A peripheral
disorder is likely if nystagmus increases on covering the fixating eye. In the ophthalmoscopic examination,
the direction of nystagmus appears reversed, because the optic nerve head is behind the center of eye
rotation [26].
● Testing nystagmus in different gaze positions can provide other localizing clues. In peripheral lesions, the
predominant direction of nystagmus remains the same in all directions of gaze. Nystagmus that reverses
direction when the patient looks right then left suggests a central abnormality [24]. However, the absence of
this feature does not rule out a central cause of vertigo. Nystagmus that reverses direction with convergence
also suggests a central lesion.
Balance and gait — The ability to stand or walk unsupported and the direction of falling may provide useful
clues to the origin of vertigo, although it may be difficult to persuade a patient with severe vertigo to attempt to
walk.
Unilateral peripheral disorders generally cause patients to lean or fall toward the side of the lesion. Patients may
be uncomfortable and reluctant to move because of their vertigo, but they are still able to walk. Romberg testing
will cause the patients to fall or tilt to one side.
Patients with an acute cerebellar stroke are often unable to walk without falling. The direction of tilting or falling
with Romberg testing may vary.
The sensitivity of balance testing may be increased by other variables such as eye-closing, standing on foam,
and performing head movements [27].
Other neurologic signs — A careful neurologic examination should be performed since the presence of
additional neurologic abnormalities strongly suggests the presence of a central lesion. A search should be made
for cranial nerve abnormalities, motor or sensory changes, dysmetria, or abnormal reflexes. (See "The detailed
neurologic examination in adults".) In particular, the abnormal facial sensation, ptosis, and diplopia of a lateral
medullary infarction may be overlooked by both patients and clinicians when the vertigo is profound. (See
"Pathophysiology, etiology, and differential diagnosis of vertigo", section on 'Wallenberg syndrome' and "Posterior
circulation cerebrovascular syndromes", section on 'Lateral medullary infarction'.)
However, the absence of other neurologic signs does not exclude a central process. In particular, a midline or
inferior cerebellar infarction may produce no neurologic signs other than nystagmus and gait instability on
examination.
Office hearing tests — Bedside tests of hearing and an examination of the tympanic membrane can be
useful in distinguishing the etiology of vertigo. The otoscopic examination provides evidence of acute or chronic
otitis media.
The examiner can easily test hearing by several methods. One is to softly whisper into each ear and then ask the
patient to repeat what was whispered. Another is to hold the examiner's hands next to the patient's ears but out
of the patient's eyesight. The examiner then rubs the fingers together on one side, with a sham rubbing
movement on the opposite side, and asks the patient to report when the finger scratching sound is heard and
from which ear it is heard. Another method is to vibrate a 512 Hz tuning fork, placing it close to one ear and then
the other in rapid succession so that the patient can compare the loudness.
The Weber and Rinne tests are used to distinguish conductive and sensorineural hearing loss (table 4):
● In the Weber test, a vibrating tuning fork is placed on the forehead in the midline. With normal hearing, the
sound is heard equally in both ears. With sensorineural hearing loss, the sound localizes to the normal ear.
With conductive hearing loss, the sound localizes to the affected ear (figure 1 and table 4)
● The Rinne test looks for conductive hearing loss. The tuning fork is placed on the mastoid bone behind the
ear of the affected side in order to test bone conduction of sound. The vibrating tuning fork is then placed
about 2.5 cm from the ear to test air conduction. Normally, air conduction of sound is better than bone
conduction, and the sound is heard louder next to the ear than when placed on the mastoid. With conductive
hearing loss, the tuning fork is heard less well or not at all when the tuning fork is adjacent to the ear. With
sensorineural hearing loss, both air and bone conduction may be quantitatively decreased, but air
conduction remains better than bone conduction (figure 1 and table 4).
Unilateral sensorineural hearing loss suggests a peripheral lesion; audiometry is required for confirmation. If no
obvious cause of unilateral sensorineural hearing loss (eg, Meniere disease) has been identified by history, a
magnetic resonance imaging (MRI) or CT (computed tomography) scan of the posterior fossa and internal
auditory canal is necessary. (See "Evaluation of hearing loss in adults".)
While associated hearing loss strongly points to a peripheral origin of vertigo, the absence of hearing loss has
less localizing value.
Dix-Hallpike maneuver — Positional maneuvers are designed to reproduce vertigo and elicit nystagmus in
patients with a history of positional dizziness. These maneuvers are most useful in patients who do not have
symptoms or nystagmus at rest. The Dix-Hallpike maneuver tests for canalithiasis of the posterior semicircular
canal, which is the most common cause of benign paroxysmal positional vertigo (BPPV) [10]. Other maneuvers
are used to provoke the nystagmus of less common variants of BPPV (anterior canal, horizontal canal). These
are discussed separately. (See "Benign paroxysmal positional vertigo", section on 'Response to provoking
maneuvers'.)
With the patient sitting, the neck is extended and turned to one side. The patient is then placed supine rapidly, so
that the head hangs over the edge of the bed. The patient is kept in this position until 30 seconds have passed if
no nystagmus occurs. The patient is then returned to upright, observed for another 30 seconds for nystagmus,
and the maneuver is repeated with the head turned to the other side (figure 2). A video demonstrating this
maneuver can be viewed at http://www.neurology.org/content/70/22/2067/suppl/DC2 (video 1).
The Dix-Hallpike maneuver will usually provoke paroxysmal vertigo and nystagmus if posterior canal dysfunction
is present in the lower ear. The nystagmus and vertigo usually appear after a latency of a few seconds and last
less than 30 seconds. It has a typical trajectory, beating upward and torsionally, with the upper poles of the eyes
beating toward the ground. After the patient sits up, the nystagmus will recur but in the opposite direction. The
maneuver should be repeated to the same side; with each repetition the intensity and duration of nystagmus will
diminish, confirming the fatigable nature of the phenomenon. However, repetition of the maneuver can interfere
with the ability to immediately perform a therapeutic particle repositioning maneuver; repetition may be deferred
when this is being considered. (See "Benign paroxysmal positional vertigo", section on 'Particle repositioning
maneuvers'.)
The latency, transience, and fatigability, coupled with the typical mixed horizontal/rotatory direction, are important
in diagnosing benign paroxysmal positional vertigo due to posterior canalithiasis (table 5) [14]. Deviation from
these features may occur with rarer types of peripheral positional vertigo but should also raise suspicion of a
central lesion. The sensitivity of the Dix-Hallpike maneuver in patients with posterior canal BPPV ranges from
has been estimated to be as high as 88 percent [28]. (See "Benign paroxysmal positional vertigo".)
Head impulse test — The head impulse test (or head thrust test) is performed by instructing the patient to
keep his or her eyes on a distant target while wearing his usual prescription eyeglasses. The head is then turned
quickly and unpredictably by the examiner, about 15º; the starting position should be about 10º from straight
ahead.
The normal response is that the eyes remain on the target (figure 3). The abnormal response is that the eyes are
dragged off of the target by the head turn (in one direction), followed by a saccade back to the target after the
head turn; this response indicates a deficient vestibuloocular reflex (VOR) on the side of the head turn, implying
a peripheral vestibular lesion (inner ear or vestibular nerve) on that side [15,29]. Use of videonystagmography
can aid in the interpretation and accuracy of this test [30].
For distinguishing vestibular dysfunction from nonvestibular dizziness, the head impulse test is reported to have
a higher specificity (82 to 100 percent) than sensitivity (34 to 39 percent) [31-33]. However, the use of caloric
testing as the gold standard in these studies may not be appropriate and may underestimate sensitivity [34]. In
one report, flexing the head forward 30º during the test increased sensitivity to as high as 71 to 84 percent [35].
In one case series, head impulse tests were abnormal in all 14 patients with aminoglycoside vestibulotoxicity
[36].
An abnormal head impulse test is reported to be a useful test to distinguish between central and peripheral
vertigo, particularly in the setting of acute prolonged vertigo, when the examiner is trying to differentiate between
vestibular neuritis and cerebellar infarction [15,29,30]. The head impulse test is normal in most patients with
isolated cerebellar lesions (31 of 34 in one series) [37]. It is important to note that a peripheral injury may result
from infarction to the inner ear or eighth cranial nerve [24]. (See "Vestibular neuritis and labyrinthitis", section on
'Clinical manifestations'.)
Other vestibular signs — Other signs of vestibular dysfunction can be elicited on examination. The clinical
and diagnostic utility of most of these signs is not known, as they have not been systematically studied against a
gold standard.
These tests are often categorized as to those indicating static vestibular imbalance (spontaneous nystagmus,
skew deviation, ocular tilt reaction, and tilt of the subjective visual vertical) and those indicating dynamic
vestibular imbalance. The latter implies functional impairment of the vestibuloocular reflex (VOR), which acts to
keep the line of sight steady during head movements. This can be detected clinically in four ways: head impulse
test, head shaking visual acuity, post-head shaking nystagmus, and caloric tests.
● Skew deviation — A skew deviation is a vertical misalignment of the two eyes resulting from a supranuclear
(relative to the ocular motor nuclei) pathology, usually located in the brainstem [24]. This may also be
caused by a vestibular lesion because of imbalance in otolithic-ocular reflexes. The vertical separation can
be tested by placing a red lens over one eye, shining a white point-light at the patient, and asking him or her
to note the relative position of the red spot to the white spot. The light should be moved to see how the
separation changes with lateral and vertical gaze. Skew deviation is often "comitant," meaning that gaze
direction has little effect upon the distance between the images. When it is incomitant, it needs to be
differentiated from other problems such as cranial nerve IV nerve palsies. (See "Overview of diplopia".)
● HINTS examination — An examination that includes the Head Impulse test (ie, head thrust test), evaluation
for direction-changing (ie, gaze evoked) Nystagmus, and a Test of Skew has been called the HINTS
examination. The presence of any one of three clinical signs: a normal head impulse test, direction-changing
nystagmus, or a skew deviation, suggests central rather than peripheral vertigo in patients with an acute
sustained vestibular syndrome [38-42]. This is discussed in more detail separately. (See "Vestibular neuritis
and labyrinthitis", section on 'Clinical manifestations' and "Posterior circulation cerebrovascular syndromes",
section on 'Distinguishing vertigo of brainstem and cerebellar ischemia from peripheral causes'.)
● Ocular tilt reaction — The ocular tilt reaction (OTR) is a triad of skew deviation, torsional tilt of the eyes
with the upper poles tilted toward the eye that is lower, and head tilt toward the eye that is lower.
● Tilt of the subjective visual vertical — Tilt of the subjective visual vertical (SVV) is a sensitive sign of
static vestibular imbalance [43]. SVV tilt can be measured at the bedside using a simple device made from a
bucket with a straight line drawn on the bottom (picture 1) [44].
Skew deviation, OTR, and tilt of the SVV can occur with acute peripheral vestibular lesions or with acute
central lesions involving the cerebellum or brainstem vestibular pathways [45-47]. Lesions of the peripheral
vestibular system or medulla cause a skew deviation with the ipsilateral eye lower and extorted (ipsiversive),
along with an ipsiversive tilt of SVV [48]. Lesions of the midbrain cause the opposite (contraversive).
Cerebellar lesions, which involve the dentate nucleus, also cause contraversive OTR, while those that spare
the dentate nucleus can cause an ipsiversive OTR [46,49]. Patients with these manifestations may complain
of vertical diplopia but may also experience a tilt illusion of their vision [26].
● Head shaking visual acuity — Head shaking visual acuity is tested by having the patient look at an eye
chart in the distance wearing his or her customary distance vision eyeglasses. Customary eyeglasses are
important since the VOR is calibrated for a given rotational magnification that varies with different strengths
of glasses. The patient reads the eye chart while his or her head is shaken continuously over a small range
at about 2 Hz. Then, the patient reads the chart again while his or her head is still. Head shaking acuity that
is more than four lines worse than the head still acuity indicates a poor VOR.
● Head shaking nystagmus — Head shaking nystagmus is elicited by the patient shaking the head from side
to side for 15 to 40 seconds with eyes closed or Frenzel lenses in place. The shaking causes vigorous
stimulation of the horizontal semicircular canals of both sides; their velocity data are stored in the
cerebellum, decaying slowly after the head stops moving. When the shaking stops, the patient then opens
his or her eyes and attempts to look straight ahead. If both sides were equally activated, the decay of
velocity information will be balanced, and the eyes will be still. If there is unilateral labyrinthine damage, the
asymmetrical neural output will generate a nystagmus that beats away from the damaged side. This test will
be normal in patients with bilateral symmetric disease, unlike rapid head thrusts or caloric responses. The
test is abnormal in patients with unilateral central vestibular lesions.
Using caloric testing as the gold standard, head shaking nystagmus has a sensitivity of 46 percent and a
specificity of 75 percent for the detection of unilateral peripheral or central vestibular lesions [50,51]. In
series of patients with vestibular neuritis, head shaking nystagmus was present in 95 to 100 percent [52,53].
Head shaking nystagmus may also differentiate central and peripheral lesions. While the induced
nystagmus is contralateral to the lesion in peripheral vestibulopathy, nystagmus produced by head shaking
in patients with medullary lesions is ipsilateral to the lesion, even in cases in which the spontaneous
nystagmus is contralateral [54].
● Caloric testing — Caloric testing is performed by infusing warm or cold water into the ear. Otoscopy should
be performed first to ensure that cerumen is not obstructing the flow of water to the tympanic membrane and
to verify that there is no tympanic membrane perforation. The head of the patient should be tilted at 30º up
from supine for optimal stimulation of the horizontal semicircular canals.
When warm water at 44ºC is infused into an ear, the normal response is nystagmus with the fast component
toward the infused ear. The opposite response occurs when cold water at 30ºC is infused; the normal
response is nystagmus with the fast component away from the cold water-infused ear.
Lack of a response to warm or cold water on one side suggests disease on that side, usually in peripheral
lesions. Central vestibular disorders may also cause caloric hyposensitivity, especially if they involve the
vestibular root entry in the medulla. This test can cause significant distress, including nausea and vomiting
in awake patients; it is rarely performed in the office evaluation of vertigo but may be useful in the vestibular
laboratory (see 'Electronystagmography and video nystagmography' below). Caloric testing is also used in
the evaluation of coma. (See "Stupor and coma in adults".)
● Others — Hyperventilation can elicit nystagmus in several central and peripheral vestibular pathologies, and
may be a particularly sensitive test in patients with cerebellopontine tumors. In one study, ipsilesional
hyperventilation-induced nystagmus was found in 84 percent of patients with cerebellopontine tumors
compared with 34 percent in other vestibular diseases [55].
Diagnostic tests — Tests that may be useful in patients with vertigo include brain
imaging,electronystagmography (ENG) and videonystagmography (VNG), vestibular evoked myogenic
potentials, audiometry, and brainstem auditory evoked potentials. The indications for this more specialized
testing (as well as indications for specialist referral) are not precise. The relatively low prevalence of serious
disorders should be balanced against their prognostic and treatment implications when deciding whether to order
these tests [28].
Brain imaging — Magnetic resonance imaging (MRI) of the brain is indicated in selected patients when the
history and examination suggest either a central cause of vertigo or a vestibular schwannoma (acoustic
neuroma) (table 3). CT scans are significantly less sensitive for the diagnosis of cerebellar infarct and for
pathologies affecting the brainstem or vestibular nerve [56]. (See "Pathophysiology, etiology, and differential
diagnosis of vertigo".)
In a patient with acute sustained vertigo, it is often difficult to distinguish between a vascular event involving the
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cerebellum and vestibular neuritis [57]. While the latter has a benign course, the former can be acutely life
threatening. A younger patient with acute sustained vertigo, with no other neurologic signs or symptoms, and
with nystagmus and an examination that is consistent with a peripheral origin (suppression with visual fixation,
falling in opposite direction to nystagmus, horizontal/torsional nystagmus) does not need immediate imaging if
there is improvement within 48 hours [14]. However, neuroimaging is indicated if the examination is not entirely
consistent with a peripheral lesion, if there are prominent risk factors for stroke, if there are neurologic signs or
symptoms, or if there is a new headache accompanying the vertigo [14,23,57].
The procedure of choice is MRI and MR angiography (MRA). MRI can detect infarction in the posterior fossa on
the first day. MRA has a specificity and sensitivity exceeding 95 percent in detecting stenosis or occlusion of the
posterior circulation [58].
Computed tomography (CT) scanning with thin cuts through the cerebellum is an alternative when MRI scanning
is not available or in patients with metallic implants. The scan is usually normal in the first hours after an infarct
and is overall a less sensitive test than MRI for early infarcts and small mass lesions. However, intraparenchymal
hemorrhage will usually be evident immediately. A brain CT scan should therefore be performed if the clinical
picture is compatible with cerebellar hemorrhage and the MRI scan is not immediately available. In one
emergency room-based study, the diagnostic yield of head CT was low compared to MRI (2 versus 16 percent)
[59].
Electronystagmography and video nystagmography — Electronystagmography (ENG) uses electrodes to

record eye movements. Videonystagmography (VNG) uses video cameras to record eye movements. These
techniques record and quantify both spontaneous and induced nystagmus. Most balance disorders centers and
many specialists use ENG or VNG to assess vestibular function and ocular motility.
Using a battery of tests such as ocular motor screening, positional testing, head impulse testing [30], caloric
testing, and rotational testing with ENG or VNG can help to discriminate between central and peripheral
etiologies. Caloric testing in the vestibular laboratory has a reasonable sensitivity for vestibular disorders, but it
does not accurately discriminate between central and peripheral vestibulopathies [60].
In general, vestibular laboratory testing is indicated when a patient's symptoms do not respond to simple
remedies such as meclizine, persist for more than one to two weeks, or are incapacitating and thus require
further diagnostic information.
Vestibular evoked myogenic potentials — Vestibular evoked myogenic potentials (VEMPs) are a new
means of assessing otolith function [61]:
● For cervical VEMPs, which assess saccular function, a loud sound is delivered to one ear while muscular
activity is recorded in the ipsilateral sternocleidomastoid muscle.
● Ocular VEMPs primarily assess utricular function and records extraocular muscle potentials during head
vibration [62].
As an example, cVEMPs are especially useful for detecting superior semicircular canal dehiscence syndrome,
which will manifest as a cVEMP with a reduced threshold [63].
Audiometry — Audiometry is more sensitive than office testing to detect hearing loss and can quantify the
loss at high and low frequencies. The audiometric battery also establishes if recruitment is present and tests for
speech discrimination.
Audiometry has limited utility in the diagnosis of patients with vertigo. While conditions such as Meniere disease
and vestibular schwannoma are said to have characteristic patterns, the audiometric battery is not truly
diagnostic of a specific disorder independently of other factors [64]. Nevertheless, the audiogram is sensitive
enough to detect unilateral hearing loss in almost all cases of vestibular schwannoma, and may be a useful
screening test for this condition [65,66]. (See "Vestibular schwannoma (acoustic neuroma)".) Also, a finding of
low frequency sensorineural hearing loss helps confirm the diagnosis of Meniere disease.
Brainstem auditory evoked potentials — Brainstem auditory evoked potentials (BAEPs) have a 90 to 95
percent sensitivity for detecting acoustic neuromas. (See "Vestibular schwannoma (acoustic neuroma)".) Any
type of sensorineural hearing loss will disrupt the pattern of sound passing from the cochlea to the brainstem;
abnormal results are therefore nonspecific [65-67]. BAEPs are no longer routinely used in the evaluation of
patients with vertigo or suspected vestibular schwannoma.
DIAGNOSTIC APPROACH — As a first step, it is important to confirm that the patient’s problem is vertigo rather
than a different form of dizziness. The features that distinguish vertigo from other forms of dizziness are
discussed separately. (See "Approach to the patient with dizziness", section on 'General approach' and
"Approach to the patient with dizziness", section on 'Vertigo'.)
There are many causes of vertigo. It is customary to organize causes of vertigo into peripheral and central
disorders, using features of nystagmus, and the presence or absence of postural instability, hearing loss or
tinnitus, and other neurologic signs (table 3). While the resulting differential diagnosis (table 1) remains broad,
some conditions are more common than others and these are typically considered first, based upon the clinical
features, as summarized in the Table. (table 2)
Another practical approach to diagnosis often starts with the time course of symptoms:
● Acute onset, sustained vertigo – Common diagnoses in this setting include vestibular neuritis,
demyelinating disease, and a stroke in the brainstem or cerebellum. Clinicians use the presence of
cerebrovascular risk factors and associated neurologic deficits to determine the relative probability of a
cerebrovascular etiology [68]. The HINTS examination, in particular the head impulse test, can also be
particularly useful in this setting to distinguish a peripheral cause of vertigo (eg, vestibular neuritis) from a
central, cerebrovascular cause. In a young patient without cerebrovascular risk factors in whom a normal
head impulse test suggests a localization within the central nervous system, multiple sclerosis might be
more likely. However, the utility of the head impulse test or the HINTS examination has not been specifically
studied in this setting. (See 'Head impulse test' above and 'Other vestibular signs' above.).
An MRI should be performed when a cerebrovascular etiology is suspected. This is discussed in detail
separately. (See "Vestibular neuritis and labyrinthitis", section on 'Differential diagnosis' and "Posterior
circulation cerebrovascular syndromes", section on 'Distinguishing vertigo of brainstem and cerebellar
ischemia from peripheral causes'.)
● Episodic vertigo – Likely diagnoses in patients with episodic vertigo depend on the duration of events as
well as the presence of associated features:
• Very brief episodes that are precipitated by predictable movements or positions of the head are often
caused by benign paroxysmal peripheral vertigo. The Dix-Hallpike maneuver can help confirm this
diagnosis. (See 'Dix-Hallpike maneuver' above and "Benign paroxysmal positional vertigo".)
• The diagnosis of episodes with a longer duration (minutes to hours) may be further distinguished by the
presence or absence of associated clinical features. As examples, associated headache suggests
migrainous vertigo; hearing loss, tinnitus, ear fullness suggest Meniere disease; and other brainstem
neurologic deficits suggest vertebrobasilar transient ischemia. The diagnosis of these conditions are
discussed separately. (See "Vestibular migraine" and "Meniere disease" and "Posterior circulation
cerebrovascular syndromes" and "Pathophysiology, etiology, and differential diagnosis of vertigo",
section on 'Brainstem ischemia'.)
A more inclusive discussion of the causes of vertigo along with characteristic clinical features and diagnosis is
discussed separately. (See "Pathophysiology, etiology, and differential diagnosis of vertigo".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and
“Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade
reading level, and they answer the four or five key questions a patient might have about a given condition. These
articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond
the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written
at the 10th to 12th grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
“patient info” and the keyword(s) of interest.)
● Basics topics (see "Patient education: Vertigo (a type of dizziness) (The Basics)")
● Beyond the Basics topics (see "Patient education: Dizziness and vertigo (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS — Vertigo is a symptom of illusory movement, most commonly of

spinning of oneself or of the environment.
● Vertigo can be caused by disorders of the peripheral vestibular system, including the vestibular labyrinth and
the vestibular portion of the eighth cranial nerve, or by lesions within the central nervous system, usually the
brainstem or cerebellum (table 1). Underlying conditions can be benign and self-limiting, or severe and life
threatening. (See "Pathophysiology, etiology, and differential diagnosis of vertigo".)
● Historical features are helpful in confirming the presence of vertigo and identifying a likely etiology. Of these,
the time course of the symptoms provides one of the best clues to the underlying pathophysiology of vertigo
(table 2). (See 'History' above and 'Diagnostic approach' above.)
• Recurrent vertigo lasting under one minute is usually benign paroxysmal positional vertigo.
• A single episode of vertigo lasting several minutes to hours may be due to migraine or to transient
ischemia of the labyrinth or brainstem.
• The recurrent episodes of vertigo associated with Meniere disease or recurrent vestibulopathy also
typically last hours but can be briefer.
• Acute onset of vertigo that is sustained can occur with vestibular neuritis, demyelinating disease
(multiple sclerosis) or a brainstem or cerebellar stroke.
● Nystagmus represents the physical manifestation of a patient's complaint of vertigo. The presence of
nystagmus helps confirm that the patient’s complaint is vertigo, rather than an alternative form of dizziness.
Its absence does not rule out vertigo. (See "Approach to the patient with dizziness", section on
'Nystagmus'.)
Features of the nystagmus: its type (horizontal, torsional, vertical), its tendency to suppress with visual
fixation, and whether or not its direction alters with gaze position can suggest a central versus peripheral
localization (table 3). (See 'Nystagmus' above.)
● Other neurologic symptoms: numbness, weakness, pronounced gait impairment, diplopia, and dysarthria
point toward a central etiology of vertigo. However, their absence does not rule out a central etiology (table
3). (See 'Postural and gait instability' above and 'Other neurologic signs' above.)
● The presence of abnormal hearing, tinnitus, or ear pain point toward a peripheral etiology of vertigo.
However, their absence does not rule out a peripheral etiology. (See 'Office hearing tests' above.)
● For patients with acute-onset sustained vertigo, an examination that includes the Head Impulse test,
evaluation for direction changing Nystagmus, and a Test of Skew (the HINTS examination) can be useful in
distinguishing peripheral from central vertigo. (See 'Other vestibular signs' above and "Vestibular neuritis
and labyrinthitis", section on 'Clinical manifestations' and "Posterior circulation cerebrovascular syndromes",
section on 'Distinguishing vertigo of brainstem and cerebellar ischemia from peripheral causes'.)
● The Dix-Hallpike maneuver is most useful to confirm the diagnosis of benign paroxysmal positional vertigo
(figure 2 and table 5). (See 'Dix-Hallpike maneuver' above.)
● Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) are indicated for patients
with suspected central causes of vertigo including those with other signs or symptoms of brainstem
dysfunction. In acute sustained vertigo, MRI or CT should be performed urgently to rule out a vascular event
in the cerebellum or brainstem in patients who are older, have vascular risk factors, have headache, and
whose examination is not completely typical of a peripheral vestibulopathy. (See 'Brain imaging' above.)
● Audiometry is useful to confirm a diagnosis of Meniere disease and to evaluate hearing loss in other causes
of peripheral vertigo. (See 'Audiometry' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 5094 Version 15.0
GRAPHICS
Causes of vertigo
Peripheral causes
Benign paroxysmal positional vertigo
Vestibular neuritis
Herpes zoster oticus (Ramsay Hunt syndrome)
Meniere disease
Labyrinthine concussion
Perilymphatic fistula
Semicircular canal dehiscence syndrome
Cogan's syndrome
Recurrent vestibulopathy
Acoustic neuroma
Aminoglycoside toxicity
Otitis media
Central causes
Vestibular migraine
Brainstem ischemia
Cerebellar infarction and hemorrhage
Chiari malformation
Multiple sclerosis
Episodic ataxia type 2
Graphic 66539 Version 8.0
Clinical features of common causes of vertigo*
Suggestive Associated Other

Time Characteristics Auditory
clinical neurologic diagnostic
course of nystagmus ¶ symptoms
setting symptoms features
Benign Recurrent, Predictable Peripheral None None Dix-Hallpike

paroxysmal brief head characteristics maneuver
positional (seconds) movements or shows
vertigo positions characteristic
precipitate findings
symptoms
Vestibular Single Viral Peripheral Falls toward Usually none Head thrust
neuritis episode, syndrome may characteristics side of lesion, test usually
acute accompany or no brainstem abnormal
onset, precede symptoms
lasts days vertigo
Meniere Recurrent Spontaneous Peripheral None Episodes may Audiometry

disease episodes, onset characteristics be preceded shows
last by ear unilateral low
minutes fullness/pain, frequency
to several accompanied sensorineural
hours by vertigo, hearing loss
unilateral
hearing loss,
tinnitus
Vestibular Recurrent History of Central or Migraine Usually none Between

migraine episodes, migraine peripheral headache episodes,
last characteristics may and/or other tests are
several be present migrainous usually
minutes symptoms normal
to hours accompanying
or following
vertigo
Vertebrobasilar Single or Older patient, Central Usually other Usually none MRI w/DWI
TIA recurrent vascular risk characteristics brainstem may
episodes factors, and or symptoms demonstrate
lasting cervical vascular
several trauma lesion
minutes
to hours
Brainstem Sudden As above Central Usually other Usually none; MRI will
infarction onset, characteristics brainstem an exception demonstrate
persistent symptoms, is anterior lesion
symptoms especially inferior
over days lateral cerebellar
to weeks medullary artery
signs syndrome
Cerebellar Sudden Older patient, Central Gait None Urgent MRI,
infarction or onset, vascular risk characteristics impairment is CT will

hemorrhage persistent factors, prominent. demonstrate
symptoms especially Headache, lesion
over days hypertension limb
to weeks dysmetria,
dysphagia
may occur
* Other diagnoses described in text "Pathophysiology and differential diagnosis of vertigo".

¶ Peripheral characteristics of nystagmus: horizontal or horizontal-torsional; suppresses with visual fixation, does not
change direction with gaze. Central characteristics of nystagmus: may be horizontal, torsional, or vertical, does not
suppress with visual fixation, may change direction with gaze.
Clinical features of central versus peripheral vertigo
Peripheral Central
Nystagmus
Direction Unidirectional, fast component toward the Sometimes reverses direction when patient
normal ear; never reverses direction looks in the direction of slow component
Type Horizontal with a torsional component, Can be any direction

never purely torsional or vertical
Effect of visual Suppressed Not suppressed

fixation
Other neurologic Absent Often present

signs
Postural Unidirectional instability, walking preserved Severe instability, patient often falls when
instability walking
Deafness or May be present Absent

tinnitus
Interpreting Weber and Rinne tests: Conductive versus sensorineural hearing loss
Weber lateralizes Rinne test
Conductive loss
Good ear AC > BC
Bad ear To bad ear BC > AC
Sensorineural loss
Good ear To good ear AC > BC
Bad ear AC > BC
AC > BC: air conduction better than bone conduction (normal Rinne).
BC > AC: bone conduction better than air conduction (abnormal Rinne).
Evaluation of hearing loss, Weber and Rinne tests
Weber test: Place the base of a struck tuning fork on the bridge of the forehead,
nose, or teeth. In a normal test, there is no lateralization of sound. With unilateral
conductive loss, sound lateralizes towards affected ear. With unilateral sensorineural
loss, sound lateralizes to the normal or better-hearing side.
Rinne test: Place the base of a struck tuning fork on the mastoid bone behind the ear.
Have the patient indicate when sound is no longer heard. Move fork (held at base)
beside ear and ask if now audible. In a normal test, AC > BC; patient can hear fork at
ear. With conductive loss, BC > AC; patient will not hear fork at ear.
Dix-Hallpike maneuver
With the patient sitting, the neck is extended and turned to one side. The
patient is then placed supine rapidly, so that the head hangs over the edge of
the bed. The patient is kept in this position and observed for nystagmus for
30 seconds. In patients with benign paroxysmal positional vertigo,
nystagmus usually appears with a latency of a few seconds and lasts less
than 30 seconds. It has a typical trajectory, beating upward and torsionally,
with the upper poles of the eyes beating toward the ground. After it stops
and the patient sits up, the nystagmus will recur but in the opposite
direction. Therefore, the patient is returned to upright and again observed
for nystagmus for 30 seconds. If nystagmus is not provoked, the maneuver
is repeated with the head turned to the other side. If nystagmus is provoked,
the patient should have the maneuver repeated to the same (provoked) side;
with each repetition, the intensity and duration of nystagmus will diminish.
Dix-Hallpike maneuver for positional nystagmus: Findings in central versus

peripheral vertigo
Peripheral disorder Central disorder
Latent period before onset of 2 to 20 seconds None

positional nystagmus
Duration of nystagmus Less than 1 minute Greater than 1 minute
Fatigability Fatiguing with repetition Nonfatiguing
Direction of nystagmus Only one type, may change May change direction with a given
direction with gaze head position
Intensity of vertigo Severe Less severe, sometimes none
Head thrust test
At rest, the patient is asked to fixate on a distant target. The patient's head is rotated
rapidly by the examiner, first to the left (A to B), then to the right (C to D). In a
normal response, the eyes remain on target (B). In an abnormal response, the eyes
are dragged off target (D), followed by a saccade back to the target (E). This
response implies a peripheral vestibular lesion on the right.
Hemispheric dome and bucket method of subjective visual

vertical testing
The bucket method for determining monocular and binocular visual vertical:
patients sit upright looking into a translucent plastic bucket so that the
bucket rims prevent any gravitational orientation clues. On the bottom inside
the bucket there is a dark, straight, diametric line. On the bottom outside
there is a perpendicular that originates from the center of a quadrant divided
into degrees with the zero line corresponding to the true vertical. For
measurement, the examiner rotates the bucket clockwise or
counterclockwise to an end position and then slowly rotates it back toward
the zero degree position. Patients indicate the position where they estimate
the inside bottom line to be truly vertical by signaling stop. The examiner
reads off the degrees on the outside scale. A total of 10 repetitions are
performed. An eye patch is used for monocular testing.
Reproduced with permission from: Zwergal A, Rettinger N, Frenzel C, et al. A bucket

of static vestibular function. Neurology 2009; 72:1689. Copyright © 2009 Lippincott
Williams & Wilkins.
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Evaluation of the patient with vertigo - UpToDate 5/03/18, 11)27 p. m.

Official reprint from UpToDate®

Prior medical history

trauma or barotrauma can cause a perilymphatic fistula.

● A family history of vertigo may suggest a rare hereditary channelopathy.

Electronystagmography and video nystagmography — Electronystagmography (ENG) uses electrodes to

SUMMARY AND RECOMMENDATIONS — Vertigo is a symptom of illusory movement, most commonly of

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continuous vertigo and dizziness. Acad Emerg Med 2013; 20:986.

Topic 5094 Version 15.0

Herpes zoster oticus (Ramsay Hunt syndrome)

Semicircular canal dehiscence syndrome

Cerebellar infarction and hemorrhage

Episodic ataxia type 2

Graphic 66539 Version 8.0

Clinical features of common causes of vertigo*

Suggestive Associated Other

Benign Recurrent, Predictable Peripheral None None Dix-Hallpike

Meniere Recurrent Spontaneous Peripheral None Episodes may Audiometry

Vestibular Recurrent History of Central or Migraine Usually none Between

Cerebellar Sudden Older patient, Central Gait None Urgent MRI,

infarction or onset, vascular risk characteristics impairment is CT will

* Other diagnoses described in text "Pathophysiology and differential diagnosis of vertigo".

Graphic 81596 Version 10.0

Clinical features of central versus peripheral vertigo

Type Horizontal with a torsional component, Can be any direction

Effect of visual Suppressed Not suppressed

Other neurologic Absent Often present

Deafness or May be present Absent

Graphic 76359 Version 4.0

Weber lateralizes Rinne test

Good ear AC > BC

Bad ear To bad ear BC > AC

Good ear To good ear AC > BC

Bad ear AC > BC

Graphic 74212 Version 6.0

Evaluation of hearing loss, Weber and Rinne tests

Graphic 58032 Version 10.0

Graphic 52232 Version 6.0

Dix-Hallpike maneuver for positional nystagmus: Findings in central versus

Peripheral disorder Central disorder

Latent period before onset of 2 to 20 seconds None

Duration of nystagmus Less than 1 minute Greater than 1 minute

Fatigability Fatiguing with repetition Nonfatiguing

Intensity of vertigo Severe Less severe, sometimes none

Graphic 73213 Version 6.0

Head thrust test

Graphic 52022 Version 4.0

Hemispheric dome and bucket method of subjective visual

Reproduced with permission from: Zwergal A, Rettinger N, Frenzel C, et al. A bucket

Graphic 66460 Version 14.0

Conflict of interest policy

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