bedside examination vertigo.pdf

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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

Introduction

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

A C U T E V E R T I G O

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: [email protected]


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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 theelderly. 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 anocular 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 withdistension 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.


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S18 S. Traccis et al.: Evaluating patients with vertigo

Central causes of vertigo

Cerebellar infarction

Central pathological causes of vertigo are less common thanperipheral 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 tovestibular 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 opticnerve 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


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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, thusallowing 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.

Suggested readings

Baloh RW, Honrubia V (1989) Clinical neurophysiology of the

vestibular system. Davis, Philadelphia

Brandt T (1998) Vertigo: its multisensory syndromes, 2nd edn.

Springer LondonLeigh RJ, Zee DS (1999) The neurology of eye movements, 3rd

edn. Davis, Philadelphia

Traccis S (1992) Il nistagmo fisiologico e patologico. Patron,

Bologna

Traccis S, Rosati G (1995) Nervo Vestibolare. In: Bergonzi P,

Massaro AR (eds) Trattato Italiano di neurologia. Verducci,

Rome, pp 60.3760.44

Traccis S, Zambarbieri D (1992) I movimenti saccadici. Patron,

Bologna

Traccis S, Zambarbieri D (1994) I movimenti di inseguimento

lento. Patron, Bologna

Traccis S, Zambarbieri D (1996) Le interazioni visuo-vestibolari.

Patron, Bologna


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