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Abstract Dizzines and vertigo are common complaints in

patients referred for neurological evaluation. With a basic

understanding of vestibular physiology and proper examina-
tion techniques, a correct diagnosis can generally be made at
the bedside. This article reviews the most common peripher-
al and central vestibular syndromes as well as the key ele-
ments of the bedside vestibular system examination.
Key words Dizzines Vestibular Ocular motor Physical
examination Nystagmus
Dizziness, vertigo, and disequilibrium are common com-
plaints in patients referred for neurological evaluation.
Because the results of a complete physical examination
and all diagnostic tests may be normal, the diagnosis
depends primarily on the history. Patients often have a
great deal of difficulty describing their symptoms. First,
an attempt should be made to elicit an exact description of
what the patient is experiencing. The most common com-
plaint is dizziness, a term that represents a wide range of
symptoms that may vary from true vertigo to more non-
specific symptoms characterized by unsteadiness or
imbalance, staggering, light-headedness, uncoordination,
or clumsiness.
Strictly defined, vertigo is an illusion of movement,
usually rotation, although patients occasionally describe a
sensation of linear displacement or tilt. Less than half of
the patients complaining of dizziness actually have verti-
go. The presence of true rotatory vertigo always indicates
an asymmetry of neural activity between the left and right
vestibular nuclei, whereas more nonspecific symptoms
suggest a whole series of other causes, including vasode-
pressor syncope, postural hypotension, cardiac dysrhyth-
mia, cerebellar dysfunction, peripheral neuropathy, hypo-
glycemia, and anxiety.
The history must define factors such as type of onset,
duration, number of episodes, and any associated audito-
ry and neurological signs. Vertigo is always temporary.
Even with a complete unilateral loss of vestibular func-
tion, vertigo always abates within a few days as central
compensation occurs. Long-standing nonspecific vertigo
is more likely to have psychogenic origins. Vertigo is
always made worse by head movements because they
accentuate any imbalance within the vestibular pathways.
Neurol Sci (2004) 24:S16S19
DOI 10.1007/s10072-004-0210-y
S. Traccis G.F. Zoroddu M.T. Zecca T. Cau M.A. Solinas R. Masuri
Evaluating patients with vertigo: bedside examination
S. Traccis () G.F. Zoroddu M.T. Zecca T. Cau
M.A. Solinas R. Masuri
U.O. Neurologia, Ospedale A. Segni, Ozieri (SS), Italy
e-mail: seb.tra@tiscalinet.it
S. Traccis et al.: Evaluating patients with vertigo S17
Peripheral causes of vertigo
Benign paroxysmal positioning vertigo
Benign paroxysmal positioning vertigo (BPPV) is the sin-
gle most common cause of vertigo, particularly in the
elderly. It has an almost certain pathogenesis, identifiable
in the detachment of otoliths and in their dislocation to the
semicircular canals. The term canalolithiasis refers to the
presence in the canal lumen of otoconial debris free to
move in the endolymph. The term cupulolithiasis is
reserved for the few cases of suspected adhesion of debris
to the cupula. Typically affected patients complain of
brief episodes of vertigo precipitated by rapid change of
head position relative to gravity. The so-called Dix-
Hallpike maneuver is the cornerstone of diagnosing the
common variety of posterior canal BPPV. The operator
turns the patients head 45 towards the right or left side
and brings the patient to a head-hanging position off the
bed. A typical response is characterized by a latent peri-
od of about 25 s, followed by vertigo, nausea, and a
mixed linear-rotatory nystagmus, with the fast phase beat-
ing toward the undermost ear or upward when gaze is
directed to the uppermost ear. The nystagmus gradually
recedes after 1040 s and ultimately abates even when the
precipitating head position is maintained. When the
patient returns to the seated position, the vertigo and nys-
tagmus may recur less violently in the opposite direction.
The horizontal canal variant of BPPV may produce hori-
zontal nystagmus when the patient is supine and the head
is quickly rolled to either side. If due to loose otoconia,
the nystagmus usually will be geotropic (beating toward
the ground). If otoconia are fixed to the cupula, the nys-
tagmus will be apogeotropic and persist. In most patients
with BPPV abnormal vestibular or auditory function can-
not be demonstrated. In a few it follows acute vestibular
neuritis or occurs during the course of a progressive inner
ear disease.
Vestibular neuritis
Acute unilateral vestibular paralysis is the third most com-
mon cause of peripheral vestibular vertigo. It is usually
ascribed to viral infection or to a parainfectious event. The
chief symptom is the acute onset of prolonged severe rota-
tory vertigo, associated with horizontal-torsional sponta-
neous nystagmus with the slow phases towards the affect-
ed ear, postural imbalance, and nausea without concomi-
tant auditory dysfunction. The nystagmus is always strict-
ly unidirectional. Bidirectional gaze-evoked nystagmus
excludes the diagnosis. The nystagmus is, to some extent,
always suppressed by visual fixation. The head impulse
test is invariably positive and shows absent lateral semi-
circular canal function on the affected side. In some
patients the disorder only affects the superior vestibular
nerve (horizontal semicircular canal paresis), which has a
separate path and its own ganglion, whereas the inferior
part (posterior semicircular canal) is spared. There is an
ocular tilt reaction characterized by ipsilateral head tilt and
an ocular skew deviation in which the eye ipsilateral to the
lesion is lower and extorted; the contralateral eye is high-
er and intorted. Patients often complain of vertical diplop-
ia but may also experience a tilt illusion of the visual
world. The condition gradually recovers naturally within
16 weeks.
Mnires disease
Mnires disease is characterized by attacks of severe
spontaneous vertigo with nausea and vomiting, a low fre-
quency tinnitus, fluctuating hearing loss, and a sense of
fullness or blockage in the affected ear. The vertigo attacks
usually last for a few hours, but the tinnitus and hearing
loss might continue for days. The tinnitus is typically
described as a roaring sound (the sound of the ocean or a
hollow seashell sound). Monosymptomatic cochlear or
vestibular manifestations are possible variants at the
beginning of the disease. Occasionally, the patients will
develop vestibular drop attacks. The most consistent
pathological finding in patients with Mnires disease is
an increase in the volume of endolymph associated with
distension of the entire endolymphatic system. Attacks of
Mnires disease must be distinguished by vestibular
migraine and vascular loop compression of the vestibular
nerve (vestibular paroxysmia).
Perilymph fistula
Perilymph fistula is associated with abnormal communica-
tion between the perilymph space and the middle ear
caused by traumatic pressure changes in either the cere-
brospinal fluid and/or the middle ear. Patients with fistula
may complain of imbalance, positional vertigo, and nys-
tagmus as well as a sudden hearing loss. Frequent triggers
are ambient pressure changes transferred to the inner ear,
certain head positions in space, head movements, or loco-
motion. In some patients perilymph fistula appears as a
sound-induced vestibular symptoms, known as the Tullio
phenomenon, either of the semicircular canal or of the
otolithic type. The disease is more often episodic than
chronic. Perilymph fistulas may resolve spontaneously, but
sometimes surgical repair is necessary.
S18 S. Traccis et al.: Evaluating patients with vertigo
Central causes of vertigo
Cerebellar infarction
Central pathological causes of vertigo are less common than
peripheral causes. Severe vertigo, mimicking labyrinthine
disease, may be an early symptom of acute cerebellar infarc-
tion in the territory of either the anterior inferior cerebellar
artery or the posterior inferior cerebellar artery. The vertigo
can result from pontomedullary brainstem ischemia near the
vestibular nuclei. If the impulse test or the caloric irrigation
evoke bilateral normal responses, vertigo of central origin
should be suspected. Acute peripheral vestibulopathy usual-
ly causes unidirectional nystagmus, with the fast phase in
the opposite direction. The nystagmus increases during gaze
in the direction of the fast phase, is suppressed by visual fix-
ation, and remains horizontal on upward gaze. By contrast,
with a cerebellar infarction the nystagmus is in the direction
of gaze and most prominently ipsilateral to the lesion and
cannot be suppressed by visual fixation. Ocular motor find-
ings are often present in brainstem disease such as upbeat or
downbeat nystagmus or dysconjugate nystagmus. If vertigo
and lateropulsion are caused by an incomplete Wallenbergs
syndrome, ipsilateral ataxia and controlateral hypalgesia are
very helpful.
Cerebellopontine angle tumors
Most cerebellopontine angle tumors arise on the vestibular
portion of the eighth nerve in the internal auditory canal.
Initially, they present with gradually progressive hearing
loss and tinnitus due to cochlear nerve compression. The
tumor produces such a gradual reduction in vestibular
function that the central compensatory mechanisms have
the capability of preventing the vertigo. Compression of
the brainstem and the vestibulocerebellum causes Bruns
nystagmus. It is a combination of low-frequency, high-
amplitude horizontal nystagmus on looking ipsilaterally
due to defective gaze holding, and a high-frequency, low-
amplitude nystagmus on looking contralaterally, due to
vestibular imbalance.
Epileptic vertigo
Vestibular cortical function has been identified in humans
in the superior lip of the intraparietal sulcus, in the poste-
rior superior portions of the temporal lobe, and in the tem-
poroparietal border regions. Vestibular epilepsy can be
secondary to focal epileptic discharges in these areas. The
patient experiences rotational or linear vertigo and tinni-
tus, and paresthesia may precede or accompany the verti-
go. Vertigo can be the predominant symptom of a simple
or complex partial sensory seizure. A focus located in
either frontal or temporal cortex may lead to rotatory
seizures volvular epilepsy, circling epilepsy character-
ized by paroxysmal walking in small circles.
Bedside neuro-otological examination
A bedside neuro-otological examination should be per-
formed to determine if any static or dynamic vestibular
imbalance is present. Spontaneous nystagmus indicates a tone
imbalance of the vestibulo-ocular reflex, which may be cen-
tral or peripheral. When peripheral in origin, as in vestibular
neuritis, it is typically suppressed by visual fixation. There are
several simple methods for achieving the latter at the bedside.
Frenzel glasses have 10+ diopter lenses that prevent fixation,
allowing vestibular nystagmus to be seen. An ophthalmo-
scope can also be used to block fixation and bring out a spon-
taneous nystagmus. When the fundus of one eye is apparent,
the patient is asked to cover the other eye with one hand. The
direction of the nystagmus is reversed because the optic nerve
head is behind the center of rotation of the eye. Occasionally
nystagmus can be seen even through closed lids. The nystag-
mus is always rotatory-horizontal beating clockwise-left or
counterclockwise-right. Pure vertical, torsional, or linear nys-
tagmus cannot be explained by involvement of a single canal
or single labyrinth and implies a central etiology.
A dynamic vestibular imbalance can be assessed by
determining the effect of head rotation on visual acuity,
observing the eye movements in response to low- and high-
frequency head rotations, and performing bedside caloric
testing. Dynamic visual acuity can be determined by pas-
sively rotating the patients head horizontally or vertically
at a frequency of about 2 Hz while reading a Snellen visu-
al acuity chart at the standard distance. A drop in acuity of
more than one line on the Snellen chart suggests an abnor-
mal VOR gain. The VOR can also be assessed with an oph-
thalmoscope by observing the stability of the optic nerve
head as the patient oscillates the head back and forth at
about 2 Hz while attempting to fix on an imagined distant
target. A normally functioning VOR will keep the optic
nerve head stable relative to the examiner. The high-fre-
quency VOR can be assessed by performing rapid head
rotations: head impulse test. The patient is asked to fix
upon a target while the examiner briskly turns the head hor-
izontally or vertically. The rotation should not be larger
than about 15, but should be of high acceleration. If the
VOR is working normally, gaze will be held steady; if not,
the patient has to perform a corrective catch-up saccade at
the end of the head movement to bring the image of the target
back to the fovea. Head-shaking nystagmus can also demon-
strate asymmetry of velocity storage that occurs as a result of
peripheral or central vestibular lesions. The patient is instruct-
ed to vigorously shake the head for 1015 s in the horizontal
S. Traccis et al.: Evaluating patients with vertigo S19
plane with the eyes closed. Upon stopping and opening the
eyes (preferably using Frenzel lenses), nystagmus usually
beats away from the side with the lesion. Bedside caloric test-
ing can be useful to determine the side of a peripheral vestibu-
lar lesion. The head of the patient is tilted 30 upward, so that
the orizontal semicircular canals are in the vertical plane, thus
allowing optimal caloric stimulation. Cool irrigation causes
nystagmus away from the ear and warm irrigation causes nys-
tagmus toward the ear. The nystagmus can be observed with
Frenzel lenses or occlusive ophthalmoscopy to eliminate fixa-
tion. Unilateral caloric hypo- or nonexcitability is found most
often in peripheral vestibular lesions, e.g., in vestibular neuri-
tis, acoustic neurinoma, or lesions of the labyrinths or vestibu-
lar nerve. Central vestibular disorders, however, may also
cause caloric hypoexcitability and mimic vestibular neuritis,
especially lesions at the root-entry zone of the vestibular nerve
(fascicular lesions) due to plaques in multiple sclerosis or
lacunar infarctions.
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edn. Davis, Philadelphia
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