General vestibular testing

Thomas Brandt*, Michael Strupp

Department of Neurology, Ludwig Maximilians University, Marchioninistr. 15, 81377 Munich, Germany

Accepted 19 August 2004

Available online 30 September 2004

Abstract

A dysfunction of the vestibular system is commonly characterized by a combination of phenomena involving perceptual, ocular motor,

postural, and autonomic manifestations: vertigo/dizziness, nystagmus, ataxia, and nausea. These 4 manifestations correlate with different

aspects of vestibular function and emanate from different sites within the central nervous system. The diagnosis of vestibular syndromes

always requires interdisciplinary thinking. A detailed history allows early differentiation into 9 categories that serve as a practical guide for

differential diagnosis: (1) dizziness and lightheadedness; (2) single or recurrent attacks of vertigo; (3) sustained vertigo; (4)

positional/positioning vertigo; (5) oscillopsia; (6) vertigo associated with auditory dysfunction; (7) vertigo associated with brainstem or

cerebellar symptoms; (8) vertigo associated with headache; and (9) dizziness or to-and-fro vertigo with postural imbalance. A careful and

systematic neuro-ophthalmological and neuro-otological examination is also mandatory, especially to differentiate between central and

peripheral vestibular disorders. Important signs are nystagmus, ocular tilt reaction, other central or peripheral ocular motor dysfunctions, or a

unilateral or bilateral peripheral vestibular deficit. This deficit can be easily detected by the head-impulse test, the most relevant bedside test

for the vestibulo-ocular reflex. Laboratory examinations are used to measure eye movements, to test semicircular canal, otolith, and spatial

perceptional function and to determine postural control. It must, however, be kept in mind that all signs and ocular motor and vestibular

findings have to be interpreted within the context of the patient’s history and a complete neurological examination.

q 2004 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

Keywords: Vestibular function; Vestibular disorders; Vertigo; Dizziness; Vestibulo-ocular reflex; Neuro-otological examination; Neuro-ophthalmological

examination; Electronystagmography; Posturography

1. Introduction

Vertigo and dizziness are among the most frequent

presenting symptoms, not only in neurology. According to a

survey of over 30,000 persons, the prevalence of vertigo and

dizziness over all ages lies around 17%; it rises to 39% in

those over 80 (Davis and Moorjani, 2003). Vertigo and

dizziness are not unique disease entities. Sometimes vertigo

is attributed to vestibular disorders, while dizziness is not

(Neuhauser and Lempert, 2004). There is no general

agreement, and visual stimuli can cause vertigo (e.g. height

vertigo or optokinetic vection) just as otolith disorders can

cause dizziness. Furthermore, central vestibular disorders

such as lateropulsion in Wallenberg’s syndrome may occur

without subjective vertigo or dizziness (Dieterich and

Brandt, 1992). Vertigo and dizziness are considered either

an unpleasant disturbance of spatial orientation or the

illusory perception of a movement of the body (spinning,

wobbling, or tilting) and/or of the surroundings. Both terms

refer to a number of multisensory and sensorimotor

syndromes of various etiologies and pathogeneses (Baloh

and Halmagyi, 1996; Brandt, 1999; Brandt et al., 2004;

Bronstein et al., 2004).

A dysfunction of the vestibular system is commonly

characterized by a combination of phenomena involving

perceptual, ocular motor, postural, and autonomic manifes-

tations: vertigo/dizziness, nystagmus, ataxia, and nausea

(Fig. 1, Brandt and Daroff, 1980). These 4 manifestations

correlate with different aspects of vestibular function and

emanate from different sites within the central nervous

system. Vertigo/dizziness itself results from a disturbance of

Clinical Neurophysiology 116 (2005) 406–426

www.elsevier.com/locate/clinph

1388-2457/$30.00 q 2004 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

doi:10.1016/j.clinph.2004.08.009

* Corresponding author. Address: Department of Neurology, University

of Munich, Klinikum Grosshadern, Marchioninistrasse 15, D-81377,

Munich, Germany. Tel.: C49 89 7095 2570; fax: C49 89 7095 8883.

E-mail address: thomas.brandt@med.uni-muenchen.de (T. Brandt).

cortical spatial orientation. Nystagmus is secondary to a

direction-specific imbalance of the VOR, which activates

brainstem neuronal circuitry. Vestibular ataxia and postural

imbalance are caused by inappropriate or abnormal

activation of monosynaptic and polysynaptic vestibular–

spinal pathways. Finally, the unpleasant autonomic

responses of nausea, vomiting, and anxiety traverse

ascending and descending vestibulo-autonomic pathways

and activate the medullary vomiting center.

This review on general vestibular testing is organized in

4 parts: first, background concepts about the malfunctioning

of the vestibular system; second, approaching the dizzy

patient; third, different clinical neuro-ophthalmological and

neuro-otological bedside tests, which are clearly illustrated

in the figures; and fourth, the laboratory examinations, e.g.

the magnetic search coil technique, electronystagmography,

video-oculography, vestibular-evoked myogenic potentials,

and posturography.

2. Background concepts

2.1. The vestibulo-ocular reflex (VOR) and the

classification of central vestibular disorders

The most important anatomical structure of the

vestibular system in the brainstem is the VOR. The

VOR has 3 major planes of action:

† horizontal head rotation about the vertical Z-axis (yaw).

† head extension or flexion about the horizontal Y-axis

(pitch).

† lateral head tilt about the horizontal X-axis (roll).

These 3 planes represent the three-dimensional space in

which the vestibular and ocular motor systems responsible

for spatial orientation, perception of self-movement,

stabilization of gaze, and postural control operate. The

neuronal circuitry of the horizontal and vertical semicircular

canals as well as the otoliths is based on a sensory

convergence that takes place within the VOR. The VOR

roughly connects a set of extraocular eye muscles that are

aligned with their primary direction of pull with the

respective spatial planes of the horizontal, anterior, and

posterior canals. The canals of both labyrinths form

functional pairs in the horizontal and vertical working

planes. In other words, the canals are excited/inhibited in

pairs: the horizontal right and left pair, and the vertical

anterior of one side along with the posterior canal of the

opposite side. The vertical planes of ‘pitch’ and ‘roll’ are a

result of the wiring connecting the two vertical canals that

are diagonal to the sagittal plane in the head. The pair of

canals function as a gauge of rotatory acceleration and react

to the rotational movements of the head in the correspond-

ing plane. The otoliths function as a gauge of gravity and

linear acceleration.

There is evidence that these 3 major planes of action of

the VOR allow a useful clinical classification of central

vestibular syndromes (Brandt, 1999). The plane-specific

vestibular syndromes are determined by ocular motor,

postural, and perceptual signs.

Yaw plane signs are horizontal nystagmus, past-pointing,

rotational and lateral body falls, horizontal deviation of

perceived straight-ahead.

Roll plane signs are torsional nystagmus, skew deviation,

ocular torsion, tilts of the head, body, and perceived vertical

(ocular-tilt reaction); see, for example, Fig. 2.

Fig. 1. Physiological vertigo (motion stimulation) and pathological vertigo (induced by lesion or stimuli) are characterized by similar signs and symptoms that

derive from the functions of the multisensory vestibular system (Brandt and Daroff, 1980).

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426 407

Pitch plane signs are upbeat or downbeat nystagmus,

forward or backward tilts and falls, vertical deviation of the

perceived straight-ahead.

2.2. Basic forms of vestibular dysfunction

Pathophysiologically, there are 3 basic forms of

vestibular dysfunction, each with its typical symptoms and

clinical signs:

† Bilateral (peripheral) loss of vestibular function. The

main symptoms are oscillopsia during head movements

(failure of the VOR), instability of gait and posture,

which increases in darkness or on uneven ground

(reduced or absent visual or somatosensory substitution

of vestibular loss), and only recently detected deficits in

spatial memory (lack of vestibular input for navigation

and spatial memory; Schautzer et al., 2003; Smith, 1997).

† Acute/subacute unilateral failure of vestibular function

(of the labyrinth, vestibular nerve, vestibular nuclei, or

central pathways), which causes a vestibular tonus

imbalance. The main symptoms are rotatory vertigo or

apparent body tilt (for a few days or weeks), nystagmus,

oscillopsia, nausea, and the tendency to fall in a direction

opposite to that of vertigo.

† Paroxysmal stimulation of the vestibular system of the

labyrinth (e.g. benign paroxysmal positioning vertigo),

the vestibular nerve (e.g. vestibular paroxysmia due to

vascular cross-compression), or the brainstem (e.g.

paroxysmal ataxia in MS). The main symptoms and

signs are short attacks of vertigo, dizziness, oscillopsia,

nystagmus, and postural imbalance.

Clinically, two major relevant areas of vestibular

dysfunction should be differentiated anatomically: periph-

eral vestibular disorders originating from the labyrinth

and/or vestibular nerve and central vestibular disorders.

Central vestibular forms of vertigo arise from lesions at the

neuronal connections between the vestibular nuclei and

the vestibular cerebellum as well as those between the

vestibular nuclei, the vestibular and ocular motor structures

of the brainstem, cerebellum, thalamus, and vestibular

cortex. On the one hand, these include clearly defined

clinical syndromes of various etiologies, for example,

upbeat or downbeat nystagmus (the quick phase of

nystagmus beats upward or downward). The occurrence of

these typical ocular motor findings in only the central

vestibular brainstem or in cerebellar disorders allows a

definite topical attribution. On the other hand, central

vestibular vertigo can also be part of a more complex

infratentorial clinical syndrome. In such cases other signs

and symptoms, such as supranuclear or nuclear ocular motor

disorders and/or other neurological brainstem signs (e.g.

Wallenberg’s syndrome), can also be observed. Vertigo/-

dizziness can manifest as attacks lasting for seconds or

minutes (vestibular migraine), for hours up to days

(brainstem infarction), or as a permanent syndrome (down-

beat nystagmus in cases of Arnold–Chiari malformation).

2.3. Semicircular canal or otolith dysfunction

There are several possible reasons why most vestibular

syndromes involve semicircular canal and otolith function.

The different receptors for perception of angular and linear

accelerations are housed in a common labyrinth. Their

peripheral (VIIIth nerve) and central (e.g. medial longitudi-

nal fascicle) pathways take the same course. Finally, there is

a convergence of otolith and semicircular canal input at all

central vestibular levels, from the vestibular nuclei to the

vestibular cortex.

Thus, most vestibular syndromes are mixed as regards

otolithic and canal function. A peripheral prototype of such

Fig. 2. Vestibular syndromes in the roll plane: Graviceptive pathways from

otoliths and vertical semicircular canals mediating vestibular function in

the roll plane. The projections from the otoliths and the vertical

semicircular canals to the ocular motor nuclei (trochlear nucleus IV,

oculomotor nucleus III, abducens nucleus VI), the supranuclear centers of

the interstitial nucleus of Cajal (INC), and the rostral interstitial nucleus of

the medial longitudinal fascicle (riMLF) are shown. They subserve VOR in

3 planes. The VOR is part of a more complex vestibular reaction which also

involves vestibular–spinal connections via the medial and lateral

vestibular–spinal tracts for head and body posture control. Furthermore,

connections to the assumed vestibular cortex (areas 2v and 3a and the

parieto-insular vestibular cortex, PIVC) via the vestibular nuclei of the

thalamus (VIM, Vce) are depicted. ‘Graviceptive’ vestibular pathways for

the roll plane cross at the pontine level OTR (skew torsion, head tilt, and tilt

of perceived vertical, SVV), which is depicted schematically on the right in

relation to the level of the lesion: ipsiversive OTR with peripheral and

pontomedullary lesions; contraversive OTR with pontomesencephalic

lesions. In vestibular thalamic lesions, the tilts of SVV may be

contraversive or ipsiversive; in vestibular cortex lesions they are most

often contraversive. OTR is not induced by supratentorial lesions above the

level of the INC (From Brandt, 1999).

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426408

a mixture is vestibular neuritis. It is mostly caused by failure

of the superior division of the vestibular nerve that

subserves the horizontal and the anterior semicircular canals

and the maculae of the utricle and the anterosuperior part of

the saccule (Balo, 2003; Buchele and Brandt, 1988; Fetter

and Dichgans, 1996; Murofushi et al. 2003). A central

prototype is Wallenberg’s syndrome, which involves the

medial and superior vestibular nuclei, where otolith and

canal input converge. This typically causes ocular and

body lateropulsion, and spontaneous torsional nystagmus

(Dieterich and Brandt, 1992).

It is, however, possible to selectively stimulate single

canals by caloric irrigation of the external auditory canal or

by the head-thrust test devised by Halmagyi and Curthoys

(Cremer et al., 1998; Halmagyi and Curthoys, 1988). The

prototype of a semicircular canal disease is benign

paroxysmal positioning vertigo of the posterior or horizon-

tal canal. Typical signs and symptoms of semicircular canal

dysfunction are rotational vertigo and deviation of

perceived straight-ahead, spontaneous vestibular nystagmus

with oscillopsia, postural imbalance in the Romberg test and

past-pointing, and nausea and vomiting, if severe. The

three-dimensional spatial direction of nystagmus and

vertigo depends on the spatial plane of the affected

semicircular canal and on whether the dysfunction is caused

by ampullofugal or ampullopetal stimulation or a unilateral

loss of afferent information. Malfunction of a single or more

than one semicircular canal can be detected by three-

dimensional analysis of spontaneous nystagmus (Bohmer

et al., 1997; Straumann and Zee, 1995), the head-thrust test

with individual semicircular canal plane head impulses

(Cremer et al., 1998), or perception of rotation (von Brevern

et al., 1997). Central vestibular syndromes may take

precedence over semicircular canal or otolith types. In

other words, ‘dynamic’, rotatory vertigo and nystagmus

represent (angular) canal function, whereas ‘static’ ocular-

tilt reaction, body lateropulsion, or tilts of the perceived

vertical represent (linear) otolithic function.

Although the pathophysiology of otolith dysfunction is

poorly understood, a disorder of otolithic function at

a peripheral or central level should be suspected if a patient

describes symptoms of falls, sensations of linear motion or

tilt, or else shows signs of specific derangements of ocular

motor and postural orienting and balancing responses

(Gresty et al., 1992). A significant number of patients

presenting to neurologists have signs and symptoms that

suggest disorders of otolithic function. Nevertheless,

diseases of the otoliths are poorly represented in our

diagnostic repertoire. Of these, posttraumatic otolith vertigo

(Brandt and Daroff, 1980) may be the most significant; the

rare otolith Tullio phenomenon may be the best studied

(Dieterich et al., 1989; Fries et al., 1993). Other examples

are vestibular drop attacks (Tumarkin’s otolithic crisis;

Baloh et al., 1990) and a number of central vestibular

syndromes that indicate tonus imbalance of graviceptive

circuits (skew deviation, ocular tilt reaction, lateropulsion,

or room-tilt illusion; Brandt, 1997; Brandt and Dieterich,

1994a; Brodsky, 2003; Tiliket et al., 1996), some of which

manifest without the sensation of dizziness or vertigo.

3. Approaching the patient

About 75% of all patients presenting with vertigo or

dizziness in a neurological dizziness unit will have one of

the 8 most common syndromes listed in Table 1. A clinician

not familiar with dizzy patients can best deepen his

knowledge by acquainting himself with these 8 most

frequently met but still challenging conditions. The

diagnosis of central vestibular disorders, however, com-

prises a variety of syndromes extending from the brainstem

to the vestibular cortex. Although most clinicians welcome

the effort being made to develop computer interview

systems for use with neuro-otological patients (O’Connor

et al., 1989) and expert systems as diagnostic aids in

otoneurology (Auramo et al., 1993; Mira et al., 1990), the

actual application of these systems in a clinical setting is

still quite limited.

Vertigo and dizziness are vexing symptoms. They are

sometimes difficult to assess because of their purely

Table 1

Relative frequency of different syndromes diagnosed in a special neurological dizziness unit (nZ4790 patients in 1989–2003)

Diagnosis Frequency (%)

Benign paroxysmal positioning vertigo 18.3 (Brandt and Steddin, 1993)

Phobic postural vertigo (PPV) 15.9 (Brandt, 1996)

Central vestibular disorders 13.5 (Brandt and Dieterich, 1994a)

Vestibular migraine 9.6 (Dieterich and Brandt, 1999; Neuhauser et al., 2001; 2004)

Vestibular neuritis 7.9 (Baloh, 2003)

Meniere’s disease 7.8 (James and Thorp, 2001)

Bilateral vestibulopathy 3.6 (Rinne et al., 1995)

Psychogenic vertigo (without PPV) 3.6

Vestibular paroxysmia 2.9 (Brandt and Dieterich, 1994b; Jannetta et al., 1984)

Perilymph fistula or superior canal dehiscence syndrome 0.4 (Minor et al., 1998)

Various other disorders 12.3

Unknown etiology 4.2

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426 409

subjective character and the variety of sensations patients

report. The sensation of spinning or rotatory vertigo is much

more specific; if it persists, it undoubtedly indicates acute

pathology of the labyrinth, the vestibular nerve, or the

caudal brainstem, which contains the vestibular nuclei. The

diagnosis and management of vertigo syndromes always

require interdisciplinary thinking combined with a careful

taking of the patient’s history. The history is still much more

important than recording eye movements and postural sway

or using brain imaging techniques.

3.1. Diagnostic criteria

The important diagnostic criteria of vestibular syn-

dromes manifesting with vertigo or dizziness are as follows:

† Type of vertigo: Rotatory vertigo as experienced when

riding a merry-go-round (e.g. vestibular neuritis) or

postural imbalance as experienced during boat trips (e.g.

bilateral vestibulopathy) or dizziness/lightheadedness

(e.g. intoxication).

† Duration of vertigo: Attacks of vertigo lasting for

seconds to minutes (e.g. vestibular paroxysmia), over

hours (e.g. Meniere’s disease, vestibular migraine),

sustained vertigo for days to a few weeks (e.g. vestibular

neuritis), attacks of postural instability from minutes to

hours (e.g. transient ischemic attacks of the brainstem or

cerebellar structures).

† Trigger/exacerbation of vertigo: No trigger (e.g. vestib-

ular neuritis), walking (e.g. bilateral vestibulopathy),

head turning (e.g. vestibular paroxysmia), head position-

ing (e.g. benign paroxysmal positioning vertigo), cough-

ing, pressing, loud sounds of a certain frequency

(perilymph fistula or superior canal dehiscence syn-

drome), or certain social situations (phobic postural

vertigo).

† Vertigo associated with auditory dysfunction, non-

vestibular neurological signs and symptoms, or

headache.

3.2. Diagnostic categories

A thorough patient history allows the early differen-

tiation of vertigo and disequilibrium disorders into 9

categories that serve as a practical guide for the differential

diagnosis.

3.2.1. Dizziness and lightheadedness (Table 2)

Most of us have experienced presyncopal dizziness at

some time when rapidly standing up from a relaxed supine

or seated position. Such an experience best exemplifies this

category (Baloh and Halmagyi, 1996), which includes

orthostatic hypotension and cardiac arrhythmias as well as

hyperventilation syndrome and panic attacks.

3.2.2. Single or recurrent attacks of (rotatory) vertigo

(Table 3)

Recurrent vertigo attacks in children which last several

seconds or minutes are most likely due to benign

paroxysmal vertigo of childhood, a migraine equivalent.

In adults short attacks of rotatory vertigo may occur in

Meniere’s disease, vestibular migraine, or transient verte-

brobasilar ischemia.

3.2.3. Sustained rotatory vertigo (Table 4)

Sustained vertigo occurs either with acute unilateral

peripheral loss of vestibular function or with pontomedul-

lary brainstem lesion near the vestibular nuclei. Vestibular

neuritis is the most frequent cause and its diagnostic

Table 2

Dizziness and lightheadedness

Presyncopal dizziness

Orthostatic dysregulation

Vasovagal attacks

Neuro-cardiogenic (pre) syncope

Cardiac arrhythmia and other heart diseases

Psychiatric illnesses

Hyperventilation syndrome

Panic attacks

Agoraphobia

Acrophobia

Phobic postural vertigo

Metabolic disorders

Hypoglycemia

Electrolyte disorders (hypercalcemia, hyponatremia)

Intoxication

Alcohol

Medication

Toxic substances

Table 3

Episodic vertigo (diseases with recurrent attacks of vertigo)

Labyrinth/vestibulo-cochlear nerve

†Meniere’s disease

†Vestibular paroxysmia

†Perilymph fistula

†Superior canal dehiscence syndrome (induced by coughing, pressing,

or loud sounds of a specific frequency, i.e. a Tullio phenomenon)

†Benign paroxysmal positioning vertigo (only during changes of

head position relative to gravity)

†Cogan’s syndrome

†Cysts or tumors of the cerebellopontine angle

Central vestibular system

†Transient vertebrobasilar ischemia

†‘Rotational vertebral artery occlusion syndrome’

†Vestibular epilepsy

†‘Room-tilt illusion’

†Paroxysmal ataxia/dysarthrophonia (multiple sclerosis)

†Episodic ataxia types 1 and 2

†Paroxysmal ‘ocular tilt reaction’

Peripheral and/or central vestibular system

†Basilar/vestibular migraine

†Benign paroxysmal vertigo of childhood

†Vertebrobasilar transient ischemia (e.g. AICA)

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426410

hallmark is unilateral hyporesponsiveness to caloric irriga-

tion. Differential diagnosis of the pathologies of sustained

central vertigo involves all acute processes of the intraaxial

infratentorial structures (involving the root entry zone of the

VIIIth nerve or the vestibular nuclei) such as multiple

sclerosis, tumors, or brainstem infarctions.

3.2.4. Positional/positioning vertigo (Table 5)

In the majority of patients presenting with this condition,

positioning vertigo is due to canalolithiasis in the posterior

semicircular canal. All central forms of positional vertigo

involve the region around the vestibular nuclei and a

neuronal loop to the cerebellar vermis (Buttner et al.,

1999a,b).

3.2.5. Oscillopsia (apparent motion of the visual scene)

(Table 6)

Patients with involuntary ocular oscillations (acquired

pendular nystagmus, downbeat or upbeat nystagmus) not

only report a worsening of visual acuity but also apparent

motion of the visual scene (Bronstein, 2004). Patients with

extraocular muscle paresis or defects of the VOR are often

unable to recognize faces or to read while walking; they

may also report oscillopsia. Either the deficiency of

compensatory eye movements (due to an inappropriate

VOR) or the deficiency of visual fixation (due to ocular

Table 4

Sustained vertigo or dizziness

Infections

Viral

Vestibular neuritis

Herpes zoster oticus

Viral neuro-labyrinthitis

Bacterial

Bacterial meningitis

Tuberculous labyrinthitis

Syphilitic labyrinthitis

Rarely

Chlamydial labyrinthitis

Lyme borreliosis

Autoimmunological inner ear diseases

Cogan’s syndrome

Neurosarcoidosis

Behcet’s disease

Cerebral vasculitis

Systemic lupus erythematosus

Polychondritis

Rheumatoid arthritis

Polyarteritis nodosa

Wegener’s granulomatosis

Giant cell arteritis

Primary antiphospholipid syndrome

Tumorous

Vestibular schwannoma

Meningeoma

Epidermoid cyst

Glomus tumor

Metastasis

Meningeosis carcinomatosa

Cholesteatoma

Vascular

Labyrinthine infarction (AICA)

Pontomedullar brainstem infarction

Vertebrobasilar ectasia

Hyperviscosity syndrome

Traumatic

Temporal bone fracture (transverseOlongitudinal fracture)

Labyrinthine concussion

Posttraumatic otolith vertigo

Perilymph fistula

Superior canal dehiscence syndrome

Brainstem concussion

Iatrogenic

Temporal bone surgery

Systemic or transtympanic administration of aminoglycosides

Other ototoxic substances

Table 5

Positional/positioning vertigo and/or nystagmus

Elicited by changes of head position relative to gravity

†Benign paroxysmal positioning vertigo

†Positional alcohol vertigo/nystagmus

†Positional nystagmus with macroglobulinemia

†Positional ‘heavy water’ nystagmus

†Central positional nystagmus

†Positional down-beating nystagmus

†Central positioning vomiting

Elicited by lateral head rotation

†Vestibular paroxysmia

†Rotational vertebral artery occlusion syndrome

†Compression of the VIIIth nerve due to cerebellopontine angle mass

†Carotid sinus syndrome

Table 6

Oscillopsia (illusionary movements of the surroundings)

Without head movements

†Spontaneous vestibular nystagmus (e.g. in vestibular neuritis)

†Congenital nystagmus (depending on direction of gaze)

†Downbeat nystagmus

†Upbeat nystagmus

†Acquired pendular nystagmus

†Periodic alternating nystagmus

†Opsoclonus

†Ocular flutter

†Vestibular paroxysmia

†Myokymia of the superior oblique muscle (monocular)

†Paroxysmal ‘ocular-tilt reaction’

†Spasmus nutans (infants)

†Voluntary nystagmus

During head movements

†Bilateral vestibulopathy

†Disorders of the ocular motor system (peripheral or central)

†Vestibular paroxysmia

†Benign paroxysmal positioning vertigo

†Central positional/positioning vertigo

†Vestibulo-cerebellar ataxia

†Perilymph fistula

†Superior canal dehiscence syndrome

†Posttraumatic otolith vertigo

†Rotational vertebral artery occlusion syndrome

†Intoxication (e.g. anticonvulsants, alcohol)

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426 411

oscillation) causes undesired retinal image motion with

disturbing oscillopsia and sometimes unsteadiness.

3.2.6. Vertigo-associated with auditory dysfunction

(Table 7)

The presence of dizziness, vertigo, or disequilibrium

combined with sensorineural hearing loss or tinnitus

narrows down the differential diagnosis to certain peripheral

vestibular disorders. The rare central vestibular disorders

that manifest with audiovestibular symptoms are vestibular

epilepsy or caudal brainstem disorders, such as occur in

multiple sclerosis. Audiovestibular dysfunction associated

with interstitial keratitis indicates infectious or autoimmune

disease. Congenital unilateral and bilateral vestibular

disorders may be combined with sensorineural hearing loss.

3.2.7. Vertigo associated with brainstem and cerebellar

symptoms (Table 8)

Clinical studies of the differential effects of central

vestibular pathway lesions have increasingly shown that

vestibular syndromes are accurate indicators for a topo-

graphic diagnosis. Vestibular pathways run from the VIIIth

nerve and the vestibular nuclei through ascending fibers,

such as the ipsilateral or contralateral medial longitudinal

fascicle, brachium conjunctivum, or the ventral tegmental

tract to the ocular motor nuclei, the supranuclear integration

centers in the rostral midbrain, and the vestibular thalamic

subnuclei. From there they reach several cortex areas

through the thalamic projections. Another relevant ascend-

ing projection reaches the cortex from the vestibular nuclei

via the vestibular cerebellum structures, in particular the

fastigial nucleus. In the majority of cases, central vestibular

vertigo/dizziness syndromes are caused by dysfunction or a

deficit of sensory input induced by a lesion. In a small

proportion of cases they are due to pathological excitation of

various structures, extending from the peripheral vestibular

organ to the vestibular cortex. Since peripheral vestibular

disorders are always characterized by a combination of

perceptual, ocular motor, and postural signs and symptoms,

central vestibular disorders may manifest as ‘a complete

syndrome’ or as only single components. The ocular motor

aspects, for example, predominate in the syndrome of

upbeat or downbeat nystagmus. Lateral falls may occur

without vertigo in vestibular thalamic lesions (thalamic

astasia) or as lateropulsion in Wallenberg’s syndrome. Most

central vestibular syndromes have a specific locus but not a

specific etiology. The etiology may, for example, be

vascular, autoimmunological (e.g. in MS), inflammatory,

neoplastic, toxic, or traumatic.

3.2.8. Vertigo associated with headache (Table 9)

Various peripheral and central vestibular disorders are

typically associated with headache, such as basilar or

vestibular migraine. One-third of patients with vestibular

migraine, however, do not complain of headache associated

with vestibular aura deficits (Dieterich and Brandt, 1999;

Neuhauser et al., 2001).

3.2.9. Dizziness or to-and-fro vertigo with postural

imbalance

Dizziness and to-and-fro vertigo with postural imbalance

are non-specific but frequently described symptoms.

Differential diagnosis on the basis of such symptoms is

very difficult, because central and peripheral vestibular

disorders but also non-vestibular syndromes such as visual

vertigo, presyncopal faintness, or somatoform phobic

postural vertigo are all possible diagnoses in this category.

Table 7

Combination of vestibular and audiological symptoms

Meniere’s disease

Perilymph fistula or superior canal dehiscence syndrome

Vestibular paroxysmia

Cerebellopontine angle tumor

Cogan’s syndrome or other inner ear autoimmune diseases

Ear/head trauma

Pontomedullary brainstem infarct

Pontomedullary MS plaque

Labyrinthine infarct (AICA, labyrinthine artery)

Hyperviscosity syndrome

Neurolabyrinthitis

Zoster oticus

Cholesteatoma

Inner ear malformation

Vestibular epilepsy

Table 8

Vertigo with additional brainstem/cerebellar symptoms

Basilar/vestibular migraine

Intoxication

Craniocervical malformations (e.g. Arnold–Chiari malformation)

Lacunar or territorial infarcts

Hemorrhages (e.g. cavernoma)

Inflammation (e.g. MS plaque)

Brainstem encephalitis

Head trauma

Tumors of the cerebellopontine angle, brainstem, or cerebellum

Episodic ataxia type 2

Creutzfeldt–Jakob disease

Table 9

Vertigo with headache

Migraine without aura

Basilar/vestibular migraine

Brainstem/cerebellar ischemia

Vertebrobasilar dissection

Infratentorial hemorrhage

Inner/middle ear infection

Head trauma (especially transverse temporal bone fracture)

Infratentorial tumor

Zoster oticus

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426412

4. Clinical neuro-ophthalmological and neuro-otological

examinations

The major aim of the neuro-ophthalmological, neuro-

otological, and neuro-orthoptic examinations is to differen-

tiate between peripheral and central vestibular forms of

dysfunction. Since the disorders underlying vertigo and

dizziness are often combined with disturbances of the ocular

motor system due to anatomical proximity, ocular motor

examination techniques (how to) are also described and an

interpretation of the typical findings and their localizing

impact or topographic determination of the lesion is given.

This non-vestibular system must always be tested in patients

suffering from vertigo and disequilibrium. Then the simple

and reliable bedside test of the vestibulo-ocular reflex, the

most important anatomical and physiological structure of

the vestibular system, is presented (Halmagyi–Curthoys

head-impulse test) (Halmagyi and Curthoys, 1988; Halma-

gyi et al., 1990) together with a recently developed test of

otolith function (‘the head-heave test’ (Ramat et al., 2001)).

Finally, positioning tests for posterior and horizontal canal

benign paroxysmal positioning vertigo (BPPV), the exam-

ination with Politzer’s balloon for perilymph fistula or

superior canal dehiscence syndrome, and the tests of stance

and gait are demonstrated. The techniques of the different

tests and their typical questions are summarized in Table 10.

4.1. Eye position and nystagmus

Clinical examination of patients with suspected vestib-

ular disorders should begin with the examination of the eyes

in 9 different positions (i.e. looking straight ahead, to the

right, left, up, down as well as diagonally right up, right

down, left up, and left down) to determine ocular alignment

(for example, a possible misalignment of the eye axes,

which may be accompanied by a head tilt, Fig. 3) (Brandt

and Dieterich, 1994a), fixation deficits, spontaneous or

fixation nystagmus (Serra and Leigh, 2002), range of

movement, and disorders of gaze-holding abilities (Buttner

and Grundei, 1995). The examination can be performed

with an object for fixation or a small rod-shaped flashlight.

In primary position one should look for periodic eye

movements, such as nystagmus (e.g. horizontal-rotatory,

suppressed by fixation as in peripheral vestibular dysfunc-

tion), vertically upward (upbeat nystagmus) (Baloh and

Yee, 1989; Fisher et al., 1983) or downward (downbeat

nystagmus syndrome) (Baloh and Spooner, 1981; Bohmer

and Straumann, 1998; Glasauer et al., 2003), or horizontal

or torsional movements with only slight suppression (or

increase) of intensity during fixation as in a central

vestibular dysfunction. A (non-vestibular) congenital nys-

tagmus (Gottlob, 1998; Maybodi, 2003) beats, as a rule,

horizontally at various frequencies and amplitudes and

Table 10

Examination procedure for ocular motor and vestibular systems

Type of examination Question

Inspection

Head, body, and posture Tilt or turn of head/body

Position of eyelids Ptosis

Eye position/motility

Position of eyes during straight-ahead gaze Misalignment in primary position, spontaneous or fixation nystagmus

Cover test Horizontal or vertical misalignment

Examination of eyes in 8 positions (binocular and monocular) Determination of extent of motility, gaze-evoked nystagmus, end-position

nystagmus

Gaze-holding function: after 10–408 in the horizontal or 10–208 in the

vertical and back to 08

Gaze-evoked nystagmus: horizontal and vertical, rebound nystagmus

Smooth pursuit movements: horizontal and vertical Smooth or saccadic

Saccades: horizontal and vertical when looking around or at targets Latency, velocity, accuracy, conjugacy

Optokinetic nystagmus (OKN): horizontal and vertical with OKN

drum or tape

Inducible, direction, phase (reversal or monocularly diagonal)

Peripheral vestibular function: clinical testing of the VOR (Halmagyi–

Curthoys test): rapid turning of the head and fixation of a stationary target

Unilateral or bilateral, peripheral vestibular (semicircular canal) deficit

Fixation suppression of the VOR: turn of head and fixation of a target

moving at same speed

Failure of fixation suppression

Examination with Frenzel’s glasses:

Straight-ahead gaze, to the right, to the left, downward, and upward Spontaneous nystagmus

Head-shaking test Provocation-induced nystagmus

Positioning and positional maneuver (with Frenzel’s glasses): to the right,

left, head-hanging position, turning about the cephalocaudal axis

Peripheral positional or positioning nystagmus, central positional

nystagmus

Posture and balance control:

Romberg’s test and simple and difficult posture and gait tests: Instability, tendency to fall

Open-closed eyes

With/without reclining the head

With/without distraction (writing numbers on the skin, doing maths

mentally)

Psychogenic/functional components

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426 413

increases during fixation. So-called square-wave jerks

(small saccades [0.5–58]) that cause the eyes to oscillate

around the primary position increasingly occur in progress-

ive supranuclear palsy or certain cerebellar syndromes

(Averbuch-Heller et al., 1999; Rascol et al., 1991; Shallo-

Hoffmann et al., 1990). Ocular flutter (intermittent rapid

bursts of horizontal oscillations without an intersaccadic

interval) or opsoclonus (combined horizontal, vertical, and

torsional oscillations) occur in various disorders (Helmchen

et al., 2003; Wong et al., 2001) such as encephalitis, tumors

of the brainstem or cerebellum, intoxication, or in

paraneoplastic syndromes (Bataller et al., 2003).

The examination of the eyes with Frenzel’s glasses

(Fig. 4) is a sensitive method for detecting spontaneous

nystagmus. This can also be achieved by examining one eye

with an ophthalmoscope (while the other eye is covered) and

simultaneously checking for movements of the optic papilla

or retinal vessels (Zee, 1978) even with low, slow-phase

velocities/frequencies or square-wave jerks (small saccades

[0.5–58] that are often observed in progressive supranuclear

palsy or certain cerebellar syndromes) (Leigh and Zee,

1999). Since the retina is behind the axis of rotation of the

eyeball, the direction of any observed vertical or horizontal

movement is opposite to that of the nystagmus detected with

this method, i.e. a downbeat nystagmus causes a rapid,

upward movement of the optic papilla or retinal vessels.

After checking for possible eye movements in primary

position and the misalignment of the axes of the eyes,

the examiner should then establish the range of eye

movements monocularly and binocularly in the 8 end-

positions; deficits found here can indicate, e.g. extraocular

muscle or nerve palsy. Gaze-holding deficits (Buttner and

Grundei, 1995; Leigh and Zee, 1999) can also be

determined by examining eccentric gaze position. Use of a

small rod-shaped flashlight has the advantage that the

corneal reflex images can be observed and thus ocular

misalignments can be easily detected (note: it is important to

observe the corneal reflex images from the direction of the

illumination and to ensure that the patient attentively fixates

the object of gaze.) The flashlight also allows one to

determine whether the patient can fixate with one or both

eyes in the end-positions. This is important for detecting a

defect of gaze holding. Gaze-evoked nystagmus can only be

clearly identified when the patient fixates with both eyes. It

is most often a side effect of medication (e.g. anti-

convulsants, benzodiazepines) or toxins (e.g. alcohol).

Horizontal gaze-evoked nystagmus can indicate a structural

lesion in the area of the brainstem or cerebellum (vestibular

nucleus, nucleus prepositus hypoglossi, flocculus, i.e. the

neural eye velocity to position integrator). Vertical

gaze-evoked nystagmus is observed in midbrain lesions

involving the interstitial nucleus of Cajal (Bhidayasiri et al.,

2000; Buttner and Grundei, 1995; Leigh and Zee, 1999). A

dissociated horizontal gaze-evoked nystagmus (greater in

Fig. 3. Measurement of head tilt. An abnormal head posture to the right or

left shoulder or a constant, abnormal tilt is especially observed in patients

with (a) paresis of the oblique eye muscles, e.g. in superior oblique palsy,

the head is turned to the non-affected side to lessen diplopia, or (b) an

ocular tilt reaction due to a vestibular tonus imbalance of the VOR in roll.

As a rule, the head is tilted to the side of the lower eye. Acute unilateral

lower medullary lesions (e.g. involvement of the vestibular nuclei in

Wallenberg’s syndrome) or acute unilateral peripheral vestibular lesions

cause an ipsiversive head tilt, whereas pontomesencephalic lesions of

vestibular pathways cause a contraversive head tilt.

Fig. 4. Clinical examination with Frenzel’s glasses. The magnifying lenses

(C16 diopters) with light inside prevent visual fixation, which could

suppress spontaneous nystagmus. Frenzel’s glasses enable the clinician to

better observe spontaneous eye movements. Examination should include

spontaneous and gaze-evoked nystagmus, head-shaking nystagmus (either

the examiner turns the subject’s head or the patient is instructed to quickly

turn his head to the right and to the left about 20–30 times; the eye

movements are observed after head shaking), positioning and positional

nystagmus, as well as hyperventilation-induced nystagmus. Spontaneous

nystagmus indicates a tonus imbalance of the vestibulo-ocular reflex; if it is

caused by a peripheral lesion—as in vestibular neuritis—the nystagmus is

typically dampened by visual fixation. Head-shaking nystagmus shows a

latent asymmetry of the so-called velocity storage, which can be due to

peripheral and central vestibular disorders.

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426414

the abducting than the adducting eye) in combination with

an adduction deficit points to internuclear ophthalmoplegia

due to a defect of the medial longitudinal fascicle (MLF),

ipsilateral to the adduction deficit. Downbeat nystagmus

usually increases in eccentric gaze position and when

looking down. To examine for a so-called rebound

nystagmus the patient should gaze at least 15 s to one side

and then return the eyes to the primary position; this can

cause a transient nystagmus to appear with slow phases in

the direction of the previous eye position. Rebound

nystagmus generally indicates cerebellar dysfunction or

damage to the cerebellar pathways (Hood, 1981; Hood et al.,

1973).

4.2. Smooth pursuit

The patient is asked to visually track an object moving

slowly in horizontal and vertical directions (10–208/s) while

keeping his head stationary. Corrective (catch-up or back-

up) saccades are looked for; they indicate a smooth pursuit

gain that is too low or too high (ratio of eye movement

velocity and object velocity). Many anatomical structures

(visual cortex, motion sensitive areas MT, V5, frontal eye

fields, dorsolateral pontine nuclei, cerebellum, vestibular

and ocular motor nuclei) are involved in smooth pursuit eye

movements, which keep the image of a moving object stable

on the fovea (Buttner and Grundei, 1995; Gaymard and

Pierrot-Deseilligny, 1999; Lisberger et al., 1987; Pierrot-

Deseilligny and Gaymard, 1992). These eye movements are

also influenced by alertness, various drugs, and age. Even

healthy persons exhibit a slightly saccadic smooth pursuit

during vertical downward gaze. For these reasons a saccadic

smooth pursuit as a rule does not allow either an exact

topographical or etiological classification. Marked asymme-

tries of smooth pursuit, however, indicate a structural

lesion; strongly impaired smooth pursuit is observed in

intoxication (anticonvulsives, benzodiazepines, or alcohol)

as well as degenerative disorders involving the cerebellum

or extrapyramidal system (Gaymard and Pierrot-Deseil-

ligny, 1999; Pierrot-Deseilligny and Gaymard, 1992). A

reversal of slow smooth pursuit eye movements during

optokinetic stimulation is typical for congenital nystagmus

(see above).

4.3. Saccades

First, it is necessary to observe spontaneous saccades

triggered by visual or auditory stimuli. Then the patient is

asked to glance back and forth between two horizontal or

two vertical targets. The velocity, accuracy, and the

conjugacy of the saccades should be noted. Normal

individuals can immediately reach the target with a fast

single movement or one small corrective saccade (Botzel

et al., 1993). Slowing of saccades—often accompanied by

hypometric saccades—occurs for example with intoxication

(medication, especially anticonvulsives or benzodiazepines)

(Thurston et al., 1984) or in neuro-degenerative disorders

(Troost et al., 1974). Slowing of horizontal saccades is

generally observed in brainstem lesions; there is often a

dysfunction of the ipsilateral paramedian pontine reticular

formation (PPRF) (Gaymard and Pierrot-Deseilligny,

1999). Slowing of vertical saccades indicates a midbrain

lesion in which the rostral interstitial medial longitudinal

fascicle (riMLF) is involved, not only in ischemic

inflammatory diseases but also in neuro-degenerative

diseases, especially progressive supranuclear palsy

(Bhidayasiri et al., 2001; Burn and Lees, 2002; Kuniyoshi

et al., 2002; Troost and Daroff, 1977). Hypermetric

saccades, which can be identified by a corrective saccade

back to the object, indicate lesions of the cerebellum

(especially the vermis) or the cerebellar pathways. Patients

with Wallenberg’s syndrome make hypermetric saccades

toward the side of the lesion due to a dysfunction of the

inferior cerebellar peduncle; defects of the superior

cerebellar peduncle, conversely, lead to contralateral

hypermetric saccades (Helmchen et al., 1994; Robinson et

al., 2002). A slowing of the adducting saccade ipsilateral to

a defective MLF is pathognomonic for internuclear

ophthalmoplegia (INO) (Cremer et al., 1999; Zee, 1992).

Delayed onset saccades are mostly caused by supratentorial

cortical dysfunction (Leigh and Zee, 1999).

4.4. Vestibulo-ocular reflex

One bedside test is of special clinical importance: the

head-impulse test of Halmagyi and Curthoys (Halmagyi and

Curthoys, 1988; Halmagyi et al., 1992); it allows the

examination of the horizontal VOR. This test is closely

related to the purpose and special properties of the VOR (see

above).

Fig. 5 summarizes how to do this test and how to

interpret the findings. The test also allows examination not

only of the horizontal, but also of the vertical canals,

because they can be stimulated in specific planes and sides,

e.g. the left anterior semicircular canal can be stimulated by

moving the head in the plane of this canal downward and

observing the induced eye movements. According to our

experience, the head-impulse test is very helpful; if it gives a

pathological finding, it is not necessary to do an additional

caloric irrigation.

Testing dynamic visual acuity (subject turns his head

horizontally to the right and left with a frequency of about

1 Hz and visual acuity is determined by, e.g. the Snellen

chart) is also helpful in diagnosing bilateral vestibular

failure (Burgio et al., 1992). A decrease of visual acuity by

at least 3 lines is pathological and indicates a bilateral deficit

of the VOR.

4.5. The head-heave test for otolith testing

This is a bedside test for utricular function and the trans-

lational VOR (Ramat et al., 2001). The head of the subject

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426 415

has to be moved manually in a horizontal direction to the

right and left with brief but highly accelerated motions

(‘heaves’). The ocular response to the translation is a

compensatory eye movement to keep the target stable on

the retina. This eye movement response is asymmetrical in

patients with a unilateral peripheral vestibular lesion. For

instance, if the patient has a left-sided peripheral vestibular

lesion and his head is moved toward the affected side, the

examiner can easily observe a corrective saccade to the right.

This indicates a deficit of the translational VOR (Ramat et al.,

2001) on analogy to the ‘head thrust sign’ (Halmagyi and

Curthoys, 1988).

4.6. Positioning/positional maneuvers

All patients should also be examined with the so-called

Dix-Hallpike maneuver (Fig. 6) in order not to overlook the

most common form of vertigo, benign paroxysmal position-

ing vertigo (BPPV) (Brandt and Steddin, 1993; Schuknecht,

1969) of the posterior as well as central positioning/posi-

tional nystagmus or vertigo (Bertholon et al., 2002; Brandt,

1990; Buttner et al., 1999a,b). In addition, the ‘barbecue-

spit maneuvers’ should be performed to look for a BPPV of

the horizontal canal (Baloh et al., 1993; McClure, 1985;

Pagnini et al., 1989; Strupp et al., 1995), which is

characterized by a linear horizontal nystagmus beating in

most cases to the undermost ear (‘geotropic’), but in some

cases to the uppermost ear (Bisdorff and Debatisse, 2001).

4.7. Miscellaneous

4.7.1. Visual fixation suppression of the VOR

A disorder of visual fixation suppression of the VOR

(which as a rule occurs with smooth pursuit abnormalities,

as these two functions are mediated by common neural

pathways) (Takemori, 1983) is often observed in lesions of

the cerebellum (flocculus or paraflocculus) or of the

cerebellar pathways and in progressive supranuclear palsy

(see above). Anticonvulsants and sedatives can also impair

visual fixation of the VOR. Before testing visual fixation

suppression of the VOR, it is necessary to confirm that the

VOR is intact.

4.7.2. Head-shaking nystagmus

To test for head-shaking nystagmus (HSN), the examiner

turns the subject’s head by aboutG458 horizontally about 30

times within about 15 s or the patient does it by himself.

HSN is defined as the occurrence of at least 5 beats of

nystagmus immediately after the head-shaking maneuver,

which should be performed with Frenzel’s glasses. There is

good evidence that HSN reflects a dynamic (peripheral

and/or central vestibular) asymmetry of the velocity-storage

mechanism (Hain and Spindler, 1993; Hain et al., 1987). In

peripheral lesions, the ipsilateral dynamic VOR deficit leads

to an asymmetric accumulation within the velocity storage,

the discharge of which determines the direction of HSN,

usually toward the unaffected ear (Hain and Spindler, 1993).

Head-shaking nystagmus rarely beats toward the

affected ear; this may be related to recovery nystagmus

(‘Erholungsnystagmus’) when prior compensation becomes

inappropriately excessive as a peripheral function recovers.

Central vestibular lesions may also induce an asymmetry in

Fig. 5. Clinical examination of the horizontal vestibulo-ocular reflex (VOR)

by the head-impulse test (Halmagyi and Curthoys, 1988). To test the

horizontal VOR, the examiner holds the patient’s head between both hands,

asks him to fixate a target in front of his eyes, and rapidly and arbitrarily

turns the patient’s head horizontally to the left and then to the right. This

rotation of the head in a healthy subject causes rapid compensatory eye

movements in the opposite direction (a). In cases of unilateral labyrinthine

loss the patient is not able to generate the VOR-driven fast contraversive

eye movement and has to perform a corrective (catch up) saccade to re-

fixate the target. Part b explains the findings in a patient with a loss of the

right horizontal canal. During rapid head rotations toward the affected right

ear, the eyes move with the head to the right and the patient has to perform a

refixation saccade to the left; the latter can be easily detected by the

examiner.

Fig. 6. The so-called Dix-Hallpike maneuver is performed to determine

whether benign paroxysmal positioning vertigo (BPPV) is present. While

the patient is sitting, his head is turned by 458 to one side, and then he is

rapidly put in a supine position with head hanging over the end of the

examination couch. If a BPPV of the left posterior semicircular canal, for

example, is present, this maneuver will induce, with a certain latency, a

crescendo–decrescendo-like nystagmus, which from the patient’s view-

point beats counterclockwise toward the left ear and to the forehead. When

the patient is returned to a sitting position, the direction of nystagmus will

change.

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426416

velocity storage, which itself can produce HSN even though

the peripheral vestibular inputs are balanced. Furthermore,

horizontal head-shaking may also lead to a vertical

nystagmus due to cross-coupling of nystagmus, which is

also compatible with a central vestibular origin of HSN

(Leigh and Zee, 1999). Head-shaking nystagmus may

indicate a ‘latent’ (compensated) vestibular tonus imbal-

ance, since it has also been found in healthy control subjects

(12 of 50) (Asawavichiangianda et al., 1999).

4.7.3. Politzer’s balloon: testing for perilymph fistula or

superior canal dehiscence syndrome

Patients who report attacks of rotatory or postural vertigo

caused by changes in pressure, for example, by coughing,

pressing, sneezing, lifting, or loud noises and accompanied

by illusory movements of the environment (oscillopsia) and

instability of posture and gait with or without hearing

disturbances may suffer from perilymph fistula (Nomura,

1994) and should be tested with Politzer’s balloon. The

balloon can be used to apply positive and negative pressures

to the middle ear. One should look for eye movements,

especially nystagmus, vertigo, dizziness, oscillopsia, or

blurred vision induced by these changes in pressure. A

perilymph fistula may be caused by (a) a pathological

motility of the membrane of the oval or round window or the

ossicular chain with a hypermotility of the oval window

(Dieterich et al., 1989) or (b) bony defects in the region of

the lateral wall of the labyrinth (toward the middle ear)

together with a partial collapse of the perilymphatic space,

so-called ‘floating labyrinth’ (Nomura et al., 1992).

A bony defect toward the epidural space of the anterior

canal is the cause of the ‘dehiscence of the superior

semicircular canal,’ in which vertigo and/or eye movements

can also be induced by changes in pressure, e.g. by

Politzer’s balloon (Deutschlander et al., 2004; Minor et

al., 1998). The superior canal dehiscence syndrome can be

diagnosed by high resolution CT scan of the temporal bone

(Hirvonen et al., 2003).

4.7.4. Hyperventilation

Hyperventilation leads to alkalosis and changes in the

transmembraneous potential of cells which cause increased

excitability. It may induce a transient nystagmus in

vestibular paroxysmia, which is characterized by recurrent

but short attacks of vertigo due to a neurovascular cross-

compression of the VIIIth cranial nerve in the root entry

zone as in trigeminal neuralgia (Brandt and Dieterich,

1994b; Jannetta et al., 1984; Moller et al., 1986), and in

vestibular schwannoma (Minor et al., 1999). Downbeat

nystagmus due to cerebellar lesions may also worsen during

hyperventilation (Walker and Zee, 1999).

4.8. Stance and gait

Finally, the patient’s balance should be examined under

static conditions There are different variations of the

Romberg and one-leg stance test: feet next to each other

with eyes first open and then closed (to eliminate visual

cues); standing on one foot at a time with the head in normal

position or with reclining head (the latter creates extreme

imbalance). If a psychogenic disorder is suspected, the

examiner distracts the patient by writing numbers on her

arm or having her do maths mentally. If there is

improvement under the last condition, the stance disorder

has a psychogenic-functional origin. Another variation is

the Romberg test in tandem, during which the patient places

one foot directly in front of the other (the toes of one foot

touch the heel of the other). Excessive fore–aft, right–left, or

diagonal sway should be looked for. A peripheral vestibular

functional disorder typically causes ipsiversive falls; upbeat

and downbeat nystagmus syndromes are typically associ-

ated with increased body sway forward and backward once

the eyes are closed. The analysis of posture and gait

Table 11

Disturbance of posture and gait control in peripheral vestibular disorders

Illness Direction of deviation Pathomechanism

Vestibular neuritis Ipsiversive Vestibular tonus imbalance due to failure of the horizontal and anterior

semicircular canal and utricle (Strupp, 1999)

Benign paroxysmal positioning ver-

tigo (BPPV)

Forward and ipsiversive Ampullofugal stimulation of the posterior canal due to canalolithiasis that

leads to endolymph flow (Brandt and Steddin, 1993; Brandt et al., 1994)

Attacks of Meniere’s disease

(Tumarkin’s otolithic crisis)

Lateral ipsiversive or contraversive

(falls)

Variations of the endolymph pressure lead to an abnormal stimulation of

the otoliths and sudden vestibular–spinal tonus failure (Odkvist and

Bergenius, 1988; Schuknecht and Gulya, 1983)

Tullio phenomenon Backward, contraversive, diagonal Stimulation of the otoliths by sounds of certain frequencies, e.g. in cases

of perilymph fistulas or superior canal dehiscence syndrome (Tullio,

1927)

Vestibular paroxysmia Contraversive or in different direc-

tions

Neurovascular compression of the vestibulo-cochlear nerve and

excitation (rarely inhibition) of the vestibular nerve (Arbusow et al.,

1998; Brandt and Dieterich, 1994b)

Bilateral vestibulopathy All directions, especially forward

and backward

Failure of vestibular–spinal postural reflexes, exacerbated in the dark and

on uneven ground (Rinne et al., 1995)

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426 417

instability frequently allows differentiation between periph-

eral (Table 11) and central vestibular disorders (Table 12)

(Bronstein et al., 2004; Jacobson et al., 1993).

5. Laboratory examinations

The laboratory examinations measure:

(a) eye movements by, e.g. electronystagmography (ENG),

video-oculography, and the magnetic search coil

technique;

(b) semicircular canal function by either caloric irrigation

for the horizontal canal, rotational testing or determi-

nation of the gain of the VOR for all 3 canals by

combining the head-impulse test (see above, Fig. 5);

(c) otolith function by assessing the eye position in roll by

the laser-scanning ophthalmoscope, ocular counterroll

(a test which still has to be established for general

vestibular testing), and vestibular-evoked myogenic

potentials for saccule function;

(d) spatial perceptional function, e.g. by determining the

subjective visual vertical; and

(e) postural control by means of posturography. Figs. 9–13

and Table 4 summarize the essential neuro-ophthalmo-

logical laboratory procedures of examination, give

typical findings, indicate how to interpret them, and

describe an orthoptic examination.

Table 13 shows the advantages and disadvantages of the

different laboratory examinations in comparison with the

neuro-ophthalmological and neuro-orthoptic examinations.

Table 13

Neuro-ophthalmological examination and laboratory diagnostics for vestibular and ocular motor disorders

Technique Features Advantages Disadvantages

Neuro-ophthalmological

examination

Total range of eye movements,

horizontal, vertical (torsional)

No technical requirements, simple,

resolution !18

No recording, eye movement velocity cannot

be judged

Orthoptic examination Fundus photography, determination

of eye misalignment and psycho-

physical determination of, e.g. the

subjective visual vertical

Precise measurement with docu-

mentation, non-invasive, well-toler-

ated

Expensive apparatuses (e.g. scanning laser

ophthalmoscope)

ENG Measurement rangeG408,

resolution of 18

Non-invasive, well-tolerated even

by children, caloric stimulation

possible, widespread method

No measurement of torsional and poor

measurement of vertical movements, eyelid

artifacts, baseline drift

Video-oculography Measurement rangeG408,

resolution of 0.1–18

Non-invasive, well-tolerated, poss-

ible to measure torsion

Measurement only possible with eyes open, 3-

D analysis is still complicated and expensive

Infrared system Measurement rangeG208,

resolution of 0.18

High resolution, non-invasive Measurements only possible with open eyes,

relatively expensive, vertical measurements

poor, torsional measurements not possible

Magnetic-coil technique Measurement rangeG408,

resolution of 0.028

Best resolution of horizontal, verti-

cal, and torsional movements

(research)

Semiinvasive, unpleasant, expensive, only

with cooperative patients, maximum of

30 min, local anesthetic necessary

Vestibular-evoked

myogenic potentials

Examination of saccular function Non-invasive, well-tolerated, simple

to perform

Still moderate clinical experience has been

made, some findings in part still contradictory

Table 12

Disturbance of posture and gait control in central vestibular disorders

Illness Direction Pathomechanism

Vestibular epilepsy

(rare)

Contraversive Focal seizures due to epileptic discharges of the vestibular cortex (Brandt

and Dieterich, 1993b)

Thalamic astasia (often

overlooked)

Contraversive or ipsiversive Vestibular tonus imbalance due to posterolateral lesions of the thalamus

(Masdeu and Gorelick, 1988)

Ocular tilt reaction Contraversive with mesencephalic lesions,

ipsiversive with pontomedullary lesions

Tonus imbalance of the vestibulo-ocular reflex in the roll plane with

lesions of the vertical canals or otolith pathways (Brandt and Dieterich,

1993a)

Paroxysmal ‘ocular tilt

reaction’

Ipsiversive with mesencephalic excitation,

contraversive with pontomedullary excitation or

excitation of the vestibular nerve

Pathological excitation of the otolith or vertical canal pathways (VOR in

the roll plane) (Dieterich and Brandt, 1993b)

Lateropulsion (Wallen-

berg’s syndrome)

Ipsiversive, diagonal Central vestibular tonus imbalance (‘roll and yaw planes’) with tilt of

subjective vertical (Dieterich and Brandt, 1992)

Downbeat nystagmus

syndrome

Backward Vestibular tonus imbalance in the ‘pitch plane’ (Brandt and Dieterich,

1995)

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426418

To clarify the cause of disorders (differential diagnoses:

ischemia, hemorrhage, tumor, or inflammation) additional

imaging techniques (Casselman, 2002; Mark and Fitzgerald,

1994) are necessary: primarily cranial magnetic resonance

imaging with precise sections of the brainstem, the

cerebellopontine angle, and the labyrinth; high resolution

CT of the temporal bone, e.g. in superior canal dehiscence

syndrome or temporal bone fractures; Doppler sonography;

and in some cases also a spinal tap, auditory evoked

potentials, and audiometry. As a rule, an otolaryngologist

gives a hearing test. In connection with the main symptom

of vertigo, audiometry is especially important for

diagnosing Meniere’s disease, labyrinthitis, vestibular

schwannoma, and other diseases of the vestibulo-cochlear

nerve as well as bilateral vestibulopathy. These techniques

are not described in this review.

5.1. Measurements of eye movements/eye position

5.1.1. Electronystagmography (ENG)

To quantitatively record eye movements, two electrodes

are placed horizontally and vertically on each eye so that the

changes in the dipole between the retina and cornea, which

occur with eye movements, can be recorded (Fig. 7)

Fig. 7. Electronystagmography (ENG). (a) Placement of the electrodes for monocular recording of horizontal and vertical eye movements. The

electrophysiological basis of the ENG is the corneo-retinal dipole (a potential difference of about 1 mV). The dipole is parallel to the longitudinal axis of the

eye, with the retina or the cornea having a negative potential. Changes in this dipole between the horizontal or vertical electrodes are DC-amplified. The ENG

allows non-invasive horizontal recordings of G408 with an accuracy of about 18 and vertical recordings of G208. Major disadvantages are susceptibility to

eyeblink artifacts, electromyographic activity, and unstable baseline; torsional eye movements cannot be recorded with the ENG. (b) Rotatory chair and

rotatory drum (with vertical stripes) with an apparatus that projects a laser spot (above the patient). This setup allows recordings of eye movements under static

conditions (e.g. test for spontaneous or gaze-evoked nystagmus, saccades, pursuit, and optokinetic nystagmus) and under dynamic conditions (per- and

postrotatory nystagmus, fixation suppression of the vestibulo-ocular reflex), as well as positional and positioning testing and caloric irrigation. (c) Caloric

testing by electronystagmography. By means of caloric testing, the excitability of the individual horizontal canals can be determined and thus whether or not

they are functioning. After excluding the possibility of a lesion of the eardrum, the head of the patient is tilted 308 upward, so that the horizontal semicircular

canals approach the vertical plane. This allows optimal caloric stimulation. The outer auditory canals on each side are separately irrigated under standard

conditions with 30 8C cool and 44 8C warm water. At the same time the horizontal and vertical eye movements are recorded by means of

electronystagmography. The irrigation with 44 8C warm water causes excitation of the hair cells of the horizontal canal and slow contraversive eye movements;

the 30 8C cool water leads to an inhibition of the slow ipsiversive eye movements.

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426 419

(Furman et al., 1996; Jongkees et al., 1962). ENG also

allows documentation of the findings (important for

monitoring the course of the patient) and, for example,

exact measurements of saccade velocity and saccade

accuracy. In addition, irrigation of the external auditory

canal with 30 8C cool and 44 8C warm water (caloric

testing) can be used to detect loss of labyrinthine function

(horizontal canal). To quantify peripheral vestibular func-

tion the maximal velocity of the irrigation-induced eye

movements (peak slow phase velocity, PSPV) should be

measured; PSPV values less than 58/s are considered

pathological. Since there is considerable interindividual

variation of caloric excitability, the so-called ‘vestibular

paresis formula’ of Jongkees (Jongkees et al., 1962) is used

to compare the function of both labyrinths: (((R308CCR448C)K(L308CCL448C))/(R308CCR448CCL308CCL448C))!100, where for instance, R 308C is the PSPV

during caloric irrigation with 308C cool water. Values of

>25% asymmetry between the affected and non-affected

labyrinth are considered pathological and indicate, for

example, a unilateral peripheral vestibular disorder. This

formula allows a direct comparison of the function of the

horizontal semicircular canals of both labyrinths and is

highly reliable in detecting unilateral peripheral vestibular

loss (Fife et al., 2000). This is also a reliable parameter for

follow-up or treatment studies (Strupp et al., 2004).

Rotational chair testing requires that the subject sit on a

chair that rotates or oscillates with certain velocities/fre-

quencies, while his eye movements are being measured in

parallel by electronystagmography (or video-oculography,

see below). During longer rotations at constant speed,

however, the thus-induced rotational nystagmus resolves

(time constant about 20 s). If the rotational chair is then

suddenly stopped, postrotational nystagmus (P I) can also be

measured. The aim of rotational chair testing is to determine

the gain of the VOR, i.e. the slow component eye velocity:

head velocity (a gain of 1.0 indicates a perfect VOR). In

contrast to caloric irrigation (which tests the VOR at a

single, effectively very low frequency of 0.003 Hz),

rotational chair testing allows examination of the VOR at

different frequencies. Since rotation affects both labyrinths

simultaneously, it is not very helpful for diagnosing

unilateral vestibular hypofunction. However, it is the only

reliable test for bilateral vestibular failure (Baloh et al.,

1984a,b; Hess et al., 1985).

All in all, ENG including caloric irrigation and rotational

chair testing is the most important and clinically relevant

neuro-otological laboratory examination. Therefore, every

patient with vertigo or dizziness should be examined at least

once by this technique or by video-oculography (see 5.1.2).

Although widely used, electronystagmography has certain

limitations. The measurement of vertical eye movements is

not always reliable, especially due to artifacts of eyelid

movements. Other muscle artifacts and electronic noise

reduce its sensitivity, and there may be a baseline drift,

mainly due to the subject’s sweating (Baloh and Honrubia,

1979; Black and Hemenway, 1972).

5.1.2. Video-oculography

Video-oculography or video-nystagmography is another

non-invasive method that is now being used more frequently

(Vitte and Semont, 1995a,b; Schneider et al., 2002). It has

the same clinical relevance as ENG but is cheaper and easier

to handle. The eyes are first filmed by one or two video

cameras (i.e. monocular or binocular recording) integrated

in a mask attached to the head. Then a computer analysis of

the image of movements of the pupils and light reflexes is

performed to represent the eye movements in two dimen-

sions. This method allows rapid and reliable recording of

horizontal and vertical eye movements (without muscle

artifacts or unstable baseline). Recording is only possible

when the eyes are wide open, and the resolution is limited

due to the image repeat frequency of the video camera

(today generally limited to 100 Hz). There is a largely linear

resolution in the range of G308. The use of 3-D

representation of eye movements for research purposes

(i.e. additional measurement of torsion) requires an

extensive analysis of the image of the iritic structures or

of two additional marker dots applied to the sclera (Fig. 8)

(Schneider et al., 2002).

5.1.3. Magnetic search coil technique

The magnetic search coil technique (Fig. 9) is the gold

standard of scientific eye movement recordings for several

reasons (Bartl et al., 1996; Robinson, 1963). It allows the

recording of horizontal, vertical, and torsional eye move-

ments, i.e. in all 3 planes, including recordings of head

movements (see below). Its sensitivity is !5 min of an arc

and the drift is minimal. With the magnetic search coil

Fig. 8. Video-oculography performed with a mask attached to the head in

which a camera is integrated. An infrared headlight built into the mask also

allows measurement of eye movements in complete darkness. The signal of

the integrated camera is transmitted to a normal digital video camera and

finally stored on a PC. The pictures are analyzed offline by means of a

video-oculography program that calculates the eye movements. A Cajal dot

placed on the sclera simplifies the registration or analysis of eye movements

in the roll plane.

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426420

technique, eye movements can be recorded and analyzed

three-dimensionally and their trajectory reconstructed, thus,

the semicircular canal(s) involved can be determined. This

is important for the diagnosis of, e.g. superior canal

dehiscence syndrome (Cremer et al., 2000a,b), or detailed

analysis of BPPV (Fetter and Sievering, 2000), vestibular

neuritis (Fetter and Dichgans, 1996), isolated lesions of

certain semicircular canals (Cremer et al., 2000a,b), and

alcohol-induced nystagmus (Fetter et al., 1999).

The major disadvantage of this ‘semiinvasive’ method is

that a kind of contact lens has to be used which makes

necessary the application of topical anesthetic drops to the

cornea. These drops are rarely harmful to the cornea.

Recordings longer than 20–30 min should not be performed.

In general, the magnetic search coil technique is mainly

used as a research tool; its clinical relevance is limited.

5.1.4. Measurement of the static eye position

in the roll plane

Measurement of ocular torsion by fundus photography or

the ‘scanning laser ophthalmoscope’ (Ott and Eckmiller,

1989) (Fig. 10) is of special importance for the diagnosis of

central vestibular disorders that affect graviceptive path-

ways, e.g. the ocular tilt reaction and for the differentiation

of ocular tilt reaction (OTR) (Brandt and Dieterich, 1993a;

Dieterich and Brandt, 1993b; Strupp et al., 2003) and

trochlear palsy (Dieterich and Brandt, 1993a). This

technique has become more and more important in centers

specialized in the diagnosis and treatment of patients

suffering from vertigo or dizziness.

5.2. Measurements of the gain of the VOR and of otolith

function

5.2.1. Three-dimensional analysis of eye movements

and the VOR

Ewald’s first law predicts that the axis of the

nystagmus matches the anatomic axis of the semicircular

canal that generated it (Ewald, 1892). This law is

clinically useful when diagnosing the detailed pathology

of the vestibular end-organ. The magnetic search coil

technique (5.1.3 and Fig. 9) in combination with the head-

impulse test (4.4 and Fig. 5) allows calculation of the gain

of the VOR for each plane and thus, for each semicircular

canal (Cremer et al., 1988; Cremer et al., 2000a,b; Della-

Santina et al., 2001; Halmagyi et al., 1991; Halmagyi

et al., 1992). The involvement of certain canals, for

instance, in vestibular neuritis can be determined by this

method (Aw et al., 2001).

5.2.2. Measurement of otolith function

5.2.2.1. Vestibular-evoked myogenic potentials (VEMPs). In

response to loud clicks, a vestibular-evoked potential can be

recorded from sternocleidomastoid muscles. This is called a

‘vestibular-evoked myogenic potential’ (VEMP) (Fig. 11)

(Colebatch et al., 1994; Murofushi et al., 1996; Murofushi

et al., 2002). There is evidence that VEMPs originate in the

medial (striola) area of the saccular macula (Murofushi

et al., 1995). Therefore, they should test for otolith function

and also for central lesions, which may show pathological

latencies in case of multiple sclerosis (Murofushi et al.,

2001b). The findings for individual illnesses are as follows.

Vestibular neuritis: the VEMP is preserved in two-thirds of

the patients. This is due to the sparing of the pars inferior of

the vestibular nerve, which supplies the saccule and

posterior canal, among others (Colebatch, 2001; Murofushi

et al., 1996). Tullio phenomenon in cases of superior canal

dehiscence syndromes or perilymph fistula: here there is a

clearly lowered stimulus threshold, i.e. a stimulus reaction

occurs already at low dB values. Bilateral vestibulopathy:

Fig. 10. Measurement of the eye position in the roll plane. The scanning

laser ophthalmoscope (SLO) can be used to make photographs of the

fundus of the eye (examination is also possible with a fundus camera). The

rolling of the eye or eye torsion can be measured in degrees on the fundus

photographs as the angle between the horizontal and the so-called

papillofoveal meridian. The patient sits upright, looks into the SLO, and

fixates a dot. (It is not necessary to administer a mydriatic drug; however, it

is necessary if the measurement is made with traditional fundus

photography). Both eyes of healthy controls exhibit a slightly excyclotropic

position in the roll plane, i.e. counterclockwise rotation of the right eye,

clockwise rotation of the left eye (from the viewpoint of the examiner). The

normal range (G2 SDs) is from K1 to 11.5 degrees. Values outside this

range are considered pathological (e.g. patients with a peripheral vestibular

lesion show an ipsiversive ocular torsion).

Fig. 9. The magnetic search coil technique. Silastic annulus with imbedded

coils of fine wire is put on the cornea. The subject sits in a magnetic field

within a cage. Changes of the eye position cause a current that is amplified

and recorded, thus allowing the three-dimensional recording of eye

movements.

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426 421

the VEMP is absent in only a portion of the patients; this

should be interpreted as a sign of additional damage to the

saccular function (Colebatch, 2001; Matsuzaki and Mur-

ofushi, 2001). Meniere’s disease: the VEMPs are frequently

reduced or absent (Murofushi et al., 2001a). The clinical

relevance of VEMP for general vestibular testing has still to

be evaluated.

5.3. Psychophysical procedures

5.3.1. Measurement of the subjective visual vertical

Recent years have witnessed the growing importance of

psychophysical examination procedures, in particular the

psychophysical determination of the subjective visual

vertical (SVV) (Fig. 12) (Bohmer and Mast, 1999; Bohmer

and Rickenmann, 1995). The topographical and diagnostic

significance of these procedures is particularly evident when

differentiating between peripheral and central vestibular or

ocular motor lesions and between OTR (Brandt and

Dieterich, 1993a) and trochlear palsy (Dieterich and Brandt,

1993a). In our experience the determination of SVV is an

important clinical tool for all patients suffering from vertigo,

dizziness, or ocular motor disorders. It is easy to handle and

the findings are easy to interpret.

5.4. Posturography

Posturography allows the examination and quantification

of postural stability under different conditions, such as

standing with the eyes open/eyes closed, standing on firm

ground, or standing on a foam rubber platform (Fig. 13) and

under static or dynamic conditions (Baloh et al., 1998;

Black, 2001; Black et al., 1989; Di Fabio, 1996; Furman,

1994; Hamid et al., 1991). From the raw data (measured

changes in the center of gravity to the right, left, forward,

Fig. 11. Vestibular-evoked myogenic potentials (VEMPs). The VEMP is

used to test the reflex arc of the saccule which extends over the vestibular

nerves, vestibular nuclei, interneurons, and motor neurons to the neck

musculature (sternocleidomastoid m.). It complements caloric testing, since

the latter tests only the canal system and not the otolith function. The

prerequisite for VEMP testing is an intact middle ear function; it is not

necessary that hearing be preserved, since the ‘sensitivity to sound’ of the

saccule can be used in the VEMP. The reflex is triggered by a loud click.

Surface EMG is used to record from both sternocleidomastoid muscles. (a)

Healthy subjects first show on the ipsilateral side a positive wave (about

14 s after the stimulus) as well as a negative wave (about 21 ms; lines 1 and

3). (b) The responses can as a rule not be recorded contralaterally (lines 2

and 4). Approximately 50–100 averagings are necessary for the recording.

It is important that the musculature is tense, e.g. for this the test person can

raise his head from the support surface. Evaluation criteria are the presence

of the waves P14 and N21 as well as their amplitude. The absence of these

waves as well as a clearly reduced amplitude are considered pathological;

the relevance of changes in latency must still be determined (Recording (b)

by K. Botzel, Munich).

Fig. 12. The subjective visual vertical (SVV). For determination of the SVV,

the patient sits upright in front of a hemispheric dome (60 cm in diameter)

and looks into it. The surface of the dome extends beyond the limits of the

patient’s visual field and is covered with a random pattern of dots. This

prevents the patient from orienting himself spatially by fixed external

structures. The hemispheric dome is connected axially to a motor and can

be rotated; a circular target disk (148 of visual field) with a straight line

through the center is 30 cm in front of the patient at eye level. The line is

also connected with a DC motor and can be adjusted by the patient by

means of a potentiometer until he has the subjective impression that the line

is ‘vertical’. The deviation of the line from the objective vertical axis is

measured in degrees and registered on a PC. The mean of 10 measurements

equals the SVV. Under these conditions, the normal range (meanG2 SDs)

of the SVV is 08G2.58. Measurements can be made under static (left) and

dynamic (right) conditions.

T. Brandt, M. Strupp / Clinical Neurophysiology 116 (2005) 406–426422

backward, upward, and downward directions), different

parameters can be calculated, for example, the sway path,

sway path histograms for determining the preferential

direction of sway, or a frequency analysis can be made

(Fourier power spectra). The results of posturography are

clinically significant, e.g. for documenting the direction of

falls (lateropulsion in Wallenberg’s syndrome or thalamic

astasia) and for monitoring the course of postural instability

in degenerative cerebellar disorders or during rehabilitation.

Posturography also plays an important role in clinical

research. In the analysis of sway direction, for example, it

may indicate the side of lesion (semicircular canal or otolith

organs) and the type of dysfunction (excitation or

inhibition). It is also used to measure postural sway activity,

e.g. in phobic postural vertigo (Holmberg et al., 2003;

Querner et al., 2000), during the treatment of vestibular

disorders (Strupp et al., 1998), and after the application of

pharmacological agents such as nicotine (Pereira et al.,

2001) or other agents. Despite its applications in research,

posturography is of limited usefulness for general vestibular

testing, because the findings are often non-specific for

certain disorders and, therefore, it does not help detect the

underlying dysfunction. However, there are exceptions,

such as the characteristic 3-Hz sway in (alcohol-induced)

anterior lobe cerebellar atrophy (Diener et al., 1984) and the

pathognomonic 14–18 Hz sway in orthostatic tremor

(Yarrow et al., 2001).

Acknowledgements

We thank J. Benson for copyediting the manuscript.

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B-ENT, 2008, 4, Suppl. 8, 29-36

1. Index test

This test is performed on a seatedpatient whose eyes are closed. Theaim is to look for the presence ofpast pointing, the tendency for theoutstretched arms and fingersto drift unidirectionally. In peri-pheral vestibular disorders, lateraldeviation of the index is directedtowards the side of the lesion (ortowards the slow phase of thespontaneous nystagmus). Non-harmonious past pointing, thedeviation of only one index or ver-tical deviation suggest a centralvestibular disorder. Vertical devia-tion of the arms and fingers mayalso result from motor or proprio-ceptive disorders.

This test is mainly interestingfor the diagnosis of acute vertigo.It is useful to compare the direc-tion of the nystagmus (observedwith Frenzel spectacles) and thedirection of the postural devia-tions. Furthermore, in the case ofacute vertigo, this is the only testthat can be performed in a patientconfined to bed. On the otherhand, in a patient with chronicvertigo, a simple weakness mayinduce a deviation. Furthermore,this sign disappears progressivelyas vestibular compensation isestablished.

A dynamic variation of this test,looking at the tendency for therepetitively elevated and loweredoutstretched fingers to drift unidi-rectionally, may be performed toenhance sensitivity. Anotherdynamic variation is the finger-pointing test. It is more sensitivethan the finger-to-nose test forcerebellar dysmetria or hyperme-tria. The patient is instructed tofollow the finger of the clinicianby rapidly pointing towards eachnew position it takes.

2. Romberg test

The patient stands, feet togetherwith eyes open then closed (toeliminate visual clues) in order tocompare static balance in thesetwo states. Normally, there is nobody sway or directional fall.

In unilateral peripheral vestibu-lopathy, the patient slowly devi-ates towards the side of the lesion.This observation must be repro-ducible. In neurological pathology,postural balance is less affected byeye closure (except in sensoryataxia). However, this test is notvery sensitive, so more difficultvariations of the Romberg aredescribed:

– Jendrassik’s manoeuvre: thepatient is asked to pull both

hands in opposite directionswith the fingers linked together,resulting in an enhancement ofmuscular relaxation in thelower members.

– Romberg test in tandem: patientplaces one foot directly in frontof the other (heel to toe): thistest is very difficult and fewelderly people are able tomanage it.

– Push test: the patient is put offbalance by an antero-posteriorpush followed by a lateral push.This variation of the test isoften used if malingering is sus-pected.

– Clinician may distract thepatient by writing numbers onhis forearm if a psychologicaldisorder or malingering is sus-pected.

It is interesting to investigatehow head position influences thedirection of postural deviation aspostural reactions initiated byvestibulospinal reflexes are usual-ly opposite to the direction of thefast phase of nystagmus. Patientswith right peripheral vestibularlesion will show lateral body devi-ation towards the right. Asking thepatient to turn the head to the right(left) will result in a backward(forward) fall.

The clinical investigation of static and dynamic balance

S. Dejardin

Clinique Saint-Luc, Bouge, Belgium

Key-words. Vestibular function tests; posture; reference values; reproducibility of results

Abstract. The clinical investigation of static and dynamic balance. This article describes the clinical examination ofstatic and dynamic balance. The purpose is to illustrate the guideline for the diagnosis and management of vertigo. Formost of the tests, indicative normal values are given and discussed. The paper also looks at the clinical examination ofgait.

30 S. Dejardin

Normal values for the Rombergstanding test were reported byNyabenda et al.1 in a sample of120 healthy subjects broken downinto different age categories (ten-year brackets, with each age cate-gory including 20 subjects). Inthis study, postural deviation wasmeasured in standing subjectswith eyes closed and arms out-stretched as described by Gill etal.2 Lateral drift of the fingers wasmeasured by reference to the ver-tical axis. Lateral deviation wasconsidered to be significant ifmaintained during 30 seconds.

Significant index deviation wasfound in four subjects only: a sub-ject aged 69 years (5 cm, 5% ofthe age category) and three sub-jects in the 70-79 age category (3-10 cm, 15% of the age category).1

Romberg’s standing test wasalso investigated using craniocor-pography (CCG).3,4 The patient ismarked with lights upon both theshoulders and the head by meansof a hard hat containing markerlights above the forehead and theocciput. Lights are reflectedthrough a mirror system on theceiling into a video camera and acomputer which receives, analysesand prints the signal (a newermarking method uses ultrasoundmarkers and an ultrasound receiverunit instead of light markers).

Table 1 shows the normal valuesfor the CCG of the standing test.

Romberg’s test is a usefulmethod for studying patient withsymptomatic falls. If cerebral vas-cular hypoxia, epilepsy, cerebellarataxia, intoxication or sensori-motor loss are the main aetiologyof pathological falls, vestibulardysfunction is a significantdifferential diagnosis for thesepatients. Brandt and Dieterich5

classified central and peripheral

vestibular falls in relation to thepreferred direction of falling.

Peripheral vestibular syndromes

Vestibular neuritis results in slowfalling towards the side of thelesion.

Benign paroxysmal positioningvertigo: patients in whom attacksof vertigo are elicited by head tiltexhibit large sway amplitudes,predominantly in the fore-aftdirection. Instability decreasesprogressively in parallel with thereduction of nystagmus and verti-go.

Tumarkin’s otolithic crisis: inthis particular version of Ménière’sdisease, patients feel as if they arethrown to the ground withoutwarning. This “drop attack” is notpreceded or accompanied by verti-go. Patients remain conscious.

Otolithic Tullio phenomenon:diagonal and backwards towardsthe unaffected ear.

Bilateral vestibulopathy: insta-bility is multidirectional with thelargest amplitude in the fore-aftdirection. Patients often complainof oscillopsia associated withhead movement or when walking.

Central vestibular syndromes

Several vascular or tumour disor-ders at the level of the brainstemmay involve the central vestibular

pathway. Ipsiversive posturaldeviation usually results fromlateral medullar lesions whilecontraversive postural drift resultsfrom pontomesencephalic brain-stem lesions. Thalamic lesionsinvolve either ipsi- or contraver-sive postural deviation.

Postural imbalance is frequent-ly combined with central ocularsigns or symptoms (nystagmuswith central features, ocular tiltreaction, failure of vertical gaze,lateropulsion of the closed eyes,tilt of perceived visual vertical,Claude Bernard Horner’s syn-drome, internuclear ophtalmople-gia,…), with sensorimotor signsaffecting the limbs or cranialnerves, and with cerebellar syn-dromes. A careful examination istherefore required, since the mainapparent symptom is the patient’sinability to maintain an uprightposture.

One exception should be noted:in some cases of Wallenberg’ssyndrome, the nystagmus may behorizontal-rotatory beating in theopposite direction from posturaldeviations (“harmonious nystag-mus”).

Lesions of otholitic centralpathways or some thalamic dis-eases may occur without paresisor sensory or cerebellar deficit. Inthese cases, ocular signs are ofparticular importance.

Table 1

Normal values for the longitudinal and lateral sway as measured by craniocorpographyduring Romberg’s test. These data were derived from a neuro-otological data bank

with 10,335 normal and neuro-otological cases [Claussen CF: communication at the30th Annual Meeting of the Neurootological and Equilibriometical Society (NES)

Porto – Portugal, April 3-5, 2003]

Parameters for standing CCG Normal range – Normal range –Lower border Upper border

Longitudinal sway 1.75 cm 10.53 cmLateral sway 1.74 cm 7.06 cm

Static and dynamic balance 31

Downbeat nystagmus syn-drome is often associated with atendency to fall backwards.

Diagnostic elements

– Backward falls suggest sensoryataxia, especially when the eyesare closed. When the eyes areopen, the backward deviationsuggests frontal-lobe or fronto-pontine disorders. These fea-tures are also observed in arange of degenerative syn-dromes or in diffuse cerebralarteriosclerosis.

– Fore-aft deviations are oftenassociated with cerebellar ataxia.

– In sensory ataxia, the Rombergtest results only in slightunsteadiness when the eyes areopen. When patients close theireyes, large and disorderedoscillations occur. This con-trasts with the slow and pro-gressive deviation observed inpatients with peripheralvestibular disorders.

3. Unterberger and Fukuda’sstepping test

The stepping test initiallydescribed by Unterberger is com-monly used to assess individualswith peripheral vestibular dys-function or balance instability.Patients are required to step on thespot with arms outstretched. In theinitial form of this test, normalsubjects show no deviation orrotation while patients withperipheral vestibular dysfunctionrotate progressively towards theside of their lesion.

In 1956, Fukuda6 added a spi-der’s web drawn on the floor,within which the patients had toperform their stepping. Thismakes it possible to quantify dis-

placement after a series of50 steps. Angle of rotation (spin),angle of displacement and dis-tance of displacement are mea-sured. The most reproducibleparameter is the spin: Fukuda con-siders a rotation of more than30 degrees while stepping to bepathological.

A common variation of this testis a stepping test with the armsalongside the body. Results areglobally similar.7

However, the test-retest relia-bility of the Fukuda’s stepping testis a subject of discussion.8 Severalauthors have reported that thestepping test does not appear to beuseful for the detection of abnor-malities in the vestibular systemor for distinguishing normal indi-viduals from patients. In aprospective study of 131 normaland pathological subjects, theyfound considerable inter- andintra-individual variation in direc-tion and width of rotation and indisplacement.9 Others studiesreported the same results and con-clusions.10,11

A quantification study for theFukuda stepping test has beenpublished.1 The protocol included45 steps, with arms alongside thebody. Of 120 normal subjects indifferent age categories, only twopresented no deviation and therewere four subjects in whom therewas no spin. Subject displacementwas always forwards, never back-wards. The mean values for dis-tance of displacement, angle ofdisplacement and angle of rotationare reported in Table 2. The corre-lation between age and angle ofdeviation or angle of rotation wassignificant (r = 0.56, p <0.000).The correlation between age andforward displacement was not sig-nificant (r = 0.17, p = 0.06).Unfortunately, the authors did not

report the percentage of healthysubjects (they were all normal inthis study) who performed anabnormal test (i.e., more than 30°spin as described by Fukuda),which would be more significantfor clinical practice. However, itseems obvious from their table ofresults that this percentage alsoincreased with the age of the sub-jects.

In a study of 48 healthy sub-jects ranging from 20 to 35 years,Wintgens reported mean spinvalues of 27° (+/- 4° SD) after a50-step test (communication pre-sented at the Journées de Post-urologie, December 6-7, 2002,Brussels). During the first trial ofthe stepping test, 75% of thehealthy subjects performed theclassic Fukuda stepping test in thenormal range (defined by theseauthors as 32° spin) and 71% ofthe subjects performed a normalFukuda’s test with arms alongsidethe body (Table 3).

Using CCG, Claussen reporteda normal spin value of 82° after a100-step test.3,4

As for the reliability of the test,which was also discussed above,Nyabenda reported good test-retest reliability for body spin andangle of deviation.1 A change inthe direction of the rotation fromone test to another was onlyobserved for one subject. Reiss etal.12 reported similar results.

Wintgens also reported goodtest-retest reliability for the meanspin value and for the global per-centage of abnormal tests (com-munication presented at theJournées de Posturologie,December 6-7, 2002, Brussels). Amajor problem persists: subjectsdo not present consistently abnor-mal spin values in the first andsecond parts of the test (a subjectmay be normal (spin <32°) in the

32 S. Dejardin

first part and abnormal in the sec-ond). Table 3 contains moredetailed results.

In conclusion, it is not easy tostate a normal reference value forthe stepping test since the proto-cols described earlier are dissimi-lar. Nyabenda’s study1 clearlydemonstrates that age is an impor-tant factor to take into accountwhen interpreting the Fukuda test.The reliability and the specificityof this test are debated. So clini-cians should interpret the resultsof the stepping test with caution,especially if it is used as ascreening tool. Clinicians shouldmake different static and dynamic

tests of balance and compare theirresults in order to arrive at clearconclusions about balance in theirpatients.

4. Standard gait and star gait(Babinski-Weill test)

The standard gait test was firstdescribed by Fregly andGraybiel.13 The patient is requiredto walk 3.5 metres, with eyesclosed, in three successive runs.Deviation from the straight line ismeasured. This simple test, whichis easier than Fukuda’s test or thanthe star gait test, may be the mostuseful test for evaluating the evo-

lution of vestibular compensation.During the star gait test

(Babinsky-Weill), subjects arerequired to walk 3 to 5 steps for-wards then backwards, with theireyes closed. The star gait is aresult of the systematic unilateralpostural deviation that occurs inperipheral vestibular pathology. Itis not always easy to conduct thetest in practical terms since a largespace is required to ensure thatsubjects cannot orient themselveswithin the room.

Normative values are difficultto report since the variations in themethod are even greater than forthe stepping test. To provide anindication, the results of a studyby Nyabenda et al.1 are reported inTable 4. There is considerable cor-relation between age and devia-tion, as was seen in the steppingtest (r = 0.71; p <0.000).

5. Examination of walking

Gait examination may sometimeshelp to determine whether a pos-ture and walking disorder isinduced by a vestibular or a cen-tral disorder. Of the various neu-rology syndromes that may inducewalking difficulties, falls anddizziness are often associated withcentral vestibular and cerebellarsyndrome, with sensory ataxia,Parkinson’s syndrome and frontallesions. Gait examination startswhen the patient enters the exami-nation room. Some gait featureswould appear to be immediatelycharacteristic.

Clinical examination continueswith the patient barefoot. A care-ful observation of trunk posture,stance and walking is performed.The clinician should notice theoverall pattern of body movementduring walking, the swingingmotion of arms and legs, the

Table 2

Mean values (and standard deviation) of distance of displacement, angle of displace-ment and angle of rotation measured during a stepping test.1 The protocol included

45 steps, arms alongside the body

Forwarddisplacement (cm)

Angle of deviation(d°)

Angle of rotation(d°)

Age category Mean SD Mean SD Mean SD

20-29 60.7 30.7 19.9 7.8 13.9 6.9

30-39 62.5 26 32 10.1 23.2 10.6

40-49 71.7 35 35 12 26.7 11.3

50-59 73.3 40.7 37.8 13.4 31.9 10.6

60-69 76.2 40.2 39.1 9.8 34.7 11.4

70-79 75 33 41.5 10.9 42.1 10.1

Table 3

Number of subjects in whom spin is within the normal range (here: 32°) after the50th step in the first and second run and in the two runs, and subjects outside the nor-

mal range in the same conditions. Fukuda = arms extended; Fukuda repeat = armsalongside the body. The subjects considered to be normal or abnormal, Fukuda or

Fukuda repeat, identical in the first and second run or not, are not necessarily the samein each line

Number of subjects with abnormal spin

Test component Abnormal leftspin

Normal Abnormal rightspin

Fukuda First 5 36 7

Second 4 37 7

Identical 2 29 3

Fukuda repeat First 9 34 5

Second 5 40 3

Identical 2 29 1

Static and dynamic balance 33

regularity and the size of thestrides, the speed of walking andthe synergy of head, trunk and legmovements.

Subtle syndromes may berevealed by asking the patient tostop and go, to walk in a straightline heel-to-toe (tandem gait), towalk and turn quickly. Other spe-cial manoeuvres consist of askingthe patient to crouch, to sit and tostand up, to walk on their heelsand then to walk on tiptoe.

Akinetic-rigid gait

The classic and most common aki-netic-rigid gait disorder is seen inParkinson’s disease. Of course,falls are induced by walking diffi-culties but interestingly, late in thesyndrome, patient falls result fromthe loss of postural and rightingreflexes (that do not respond tolevodopa medication).

Patients adopt a flexed truncalposture with stooped trunk, shoul-ders and neck. Gait is slow andrigid with small paces and loss ofthe swinging of one or two arms.Tremor of the upper limbs mightbe present but is less commonlyobserved in the lower limbs.Initiating the first step is difficultso that patients begin walkingwith a few rapid, very short, shuf-fling steps (start hesitation);

sometimes patients actually stepup and down in the same placewithout any forward progress.Episodes of freezing (completecessation of movement, “feetglued to the floor”) are also typi-cally observed in patients withParkinson’s disease. Freezing mayalso be present if a doorway oranother obstacle is encountered;shuffling and freezing may berevealed if the patient is asked toturn back quickly. To maintainbalance when walking, patientsmay move forwards in a series ofvery small steps (festination)while bent forwards (subjects lookas though they are running aftertheir centre of gravity).

Cerebellar syndrome

Patients adopt a wide base stance.Backward and forward rhythmicswaying occurs. This instability isnot influenced by eye closure butis greatly increased if patientsbring their feet closer together.Gait is slow, strides are irregularand variable in timing (dyssyner-gia) and the steps are erratic asif the patients are drunk. Thisparticular gait is often observedin alcoholism (selective damageaffecting the cerebellar vermis)where legs and gait are usuallyaffected while ocular movement,

speech and upper limbs arespared. With lesions confined toone cerebellar hemisphere, anom-alies will be limited to the affectedipsilateral limb and will affectcoordination of movement morethan balance (if the vermis is notinvolved). Patients tend to falltowards the side of the lesion andthrow their leg on the affected sidetoo high and outwards. Finally, inlesions affecting the vestibular partof the cerebella, symptoms resem-ble those observed in peripheralunilateral vestibular disease.

Unilateral peripheral vestibularsyndrome

Clinicians should be attentive tosudden changes in gait directionor lateropulsion, especially ifthese abnormalities depend onhead movements. Paradoxically,lateropulsion away from the sideof the lesion may occur as a resultof voluntary efforts to correct bal-ance.

Cautious gait

Putting aside the typical casesdescribed above, it is important tonote that patients with any declinein walking ability and balancetend to develop compensationmechanisms that may disguisethe underlying problem. Thosepatients will adopt a slower gaitwith shorter and shallower steps inorder to keep contact with theground for a longer time (cautiousgait). This cautious and guardedgait is often present in the elderly.Factors contributing to a declinein the mobility of the elderly incrude degenerative joint disease,reduced range of limb mobilityand limited exercise capacity dueto cardiovascular fitness decline.Additional factors might be senso-ry deficit (vision, vestibular and

Table 4

Mean values (and standard deviation) of angle of displacement during a standard gaittest (patient are required to walk 5 m with their eyes closed in a straight line) and a

star gait test (three series of three paces forwards and backwards)

Standard gait Star gait (Babinsky Weill)

Age categories Mean (°) SD (°) Mean (°) SD (°)

20-29 10.3 4.8 1.7 0.8

30-39 18 5.6 2.3 0.7

40-49 21 7.2 2.8 1.1

50-59 23.6 10 3.4 0.8

60-69 26.3 14 4.0 1.1

70-79 28 11 4.5 0.9

34 S. Dejardin

proprioceptive function) withoutany one lesion being severeenough to explain the observedwalking difficulty. Another com-mon factor might simply be thefear of falling. Clinicians shouldnot diagnose Parkinson’s diseasein all these patients, even if someaspects of gait look similar!

In all these cases, gait examina-tion will not immediately lead to adiagnosis and a complete vestibu-lar and neurological examinationshould be performed.

7. Dynamic gait index

The Dynamic Gait Index wasdeveloped by Anne Shumway-Cook14 and has been used in olderadults to determine their likeli-hood of falling. Scores of 19 orless are related to falls in olderadults. The index tests 8 facets ofgait and can be used with an assis-tive device. Self-reported falls inthe past six months and DynamicGait Index scores have been foundto be related in persons withvestibular disorders.15 The dynamicgait index has also been used todetermine the effect of vestibularrehabilitation on the reduction offall risk in individuals with uni-lateral vestibular hypofunction.16

1. Gait level surface

Instructions: walk at your normalspeed from here to the next mark(20’)Grading: mark the lowest catego-ry that applies.(3) Normal: walks 20’, no assis-

tive devices, good speed, noevidence of imbalance, nor-mal gait pattern.

(2) Mild impairment: walks 20’,uses assistive devices, slowerspeed, mild gait deviations.

(1) Moderate impairment: walks20’, slow speed, abnormal gait

pattern, evidence of imbal-ance.

(0) Severe impairment: cannotwalk 20’ without assistance,severe gait deviations orimbalance.

2. Change in gait speed

Instructions: begin walking atyour normal pace (for 5’). When Itell you “go”, walk as fast as youcan (for 5’). When I tell you“slow”, walk as slowly as you can(for 5’).Grading: mark the lowestcategory that applies.(3) Normal: able to change

walking speed smoothly with-out loss of balance or gaitdeviation. Shows a significantdifference in walking speedsbetween normal, fast, andslow speeds.

(2) Mild impairment: is able tochange speed but demon-strates mild gait deviations, orno gait deviations but unableto achieve a significant changein velocity, or uses an assistivedevice.

(1) Moderate impairment: makesonly minor adjustments towalking speed, or accomplishesa change in speed with sig-nificant gait deviations, orchanges speed but loses sig-nificant gait deviations, orchanges speed but loses bal-ance but is able to recover andcontinue walking.

(0) Severe impairment: cannotchange speeds, or loses bal-ance and has to reach for wallor be caught.

4. Gait with horizontal headturns

Instructions: begin walking atyour normal pace. When I tell you

to “look right”, keep walkingstraight, but turn your head to theright. Keep looking to the rightuntil I tell you to “look left”, thenkeep walking straight and turnyour head to the left. Keep yourhead to the left until I tell you to“look straight” then keep walkingstraight but return your head to thecentre.Grading: mark the lowest catego-ry that applies.(3) Normal: performs head turns

smoothly with no change ingait

(2) Mild impairment: performshead turns smoothly withslight change in gait velocity,i.e., minor disruption tosmooth gait path or useswalking aid.

(1) Moderate impairment: per-forms head turns with moder-ate change in gait velocity,slows down, staggers butrecovers, can continue towalk.

(0) Severe impairment: performstask with severe disruption ofgait i.e., staggers outside 15”path, loses balance, stops,reaches for wall.

4. Gait with vertical head turns

Instructions: begin walking atyour normal pace. When I tell youto “look up”, keep walkingstraight but tip your head and lookup. Keep looking up until I tellyou, “look down”. Then keepwalking straight and turn yourhead down. Keep looking downuntil I tell you, “look straight”,then keep walking straight, butreturn your head to the centre.Grading: mark the lowest catego-ry that applies.(3) Normal: performs head turns

with no change in gait.

Static and dynamic balance 35

(2) Mild impairment: performstask with slight change in gaitvelocity i.e., minor disruptionto smooth gait path or useswalking aid.

(1) Moderate impairment: per-forms task with moderatechange in gait velocity, slowsdown, staggers but recovers,can continue to walk.

(0) Severe impairment: performstask with severe disruption ofgait i.e., staggers outside 15”path, loses balance, stops,reaches for wall.

5. Gait and pivot turn

Instructions: begin walking atyour normal pace. When I tell youto “turn and stop”, turn as quicklyas you can to face the oppositedirection and stop.Grading: mark the lowest catego-ry that applies.(3) Normal: pivot turns safely

within 3 seconds and stopsquickly with no loss of bal-ance.

(2) Mild impairment: pivot turnssafely in >3 seconds and stopswith no loss of balance.

(1) Moderate impairment: turnsslowly, requires verbal cueing,requires several small steps tocatch balance following turnand stop.

(0) Severe impairment: cannotturn safely, requires assistanceto turn and stop.

6. Step over obstacle

Instructions: begin walking atyour normal speed. When youcome to the shoebox, step over itnot around it, and keep walking.Grading: mark the lowest catego-ry that applies.(3) Normal: is able to step over

box without changing gait

speed; no evidence of imbal-ance.

(2) Mild impairment: is able tostep over box, but must slowdown and adjust steps to clearbox safely.

(1) Moderate impairment: is ableto step over box but must stop,then step over. May requireverbal cueing.

(0) Severe impairment: cannotperform without assistance.

7. Step around obstacles

Instructions: begin walking atnormal speed. When you come tothe first cone (about 6’ away),walk around the right side of it.When you come to the secondcone (6’ past first cone), Walkaround it to the left.Grading: mark the lowest catego-ry that applies.(3) Normal: is able to walk

around cones safely withoutchanging gait speed; no evi-dence of imbalance.

(2) Mild impairment: is able tostep around both cones, butmust slow down and adjuststeps to clear cones

(1) Moderate impairment: is ableto clear cones but has to slowdown significantly to accom-plish task, or requires verbalcueing.

(0) Severe impairment: unable toclear cones, walks into one orboth cones, or requires physi-cal assistance.

8. Steps

Instructions: walk up these stairsas you would at home (i.e., usingthe rail if necessary). At the top,turn around and walk down.Grading: mark the lowest catego-ry that applies.(3) Normal: alternating feet, no

rail.

(2) Mild impairment: alternatingfeet, must use rail.

(1) Moderate impairment: twofeet to a stair, must use rail.

(0) Severe impairment: cannot dosafely.

References

1. Nyabenda A, Briart C, Deggouj N,Gersdorff M. Benefit of rotationalexercises for patients with Meniere’ssyndrome, method used by the ENTdepartment of St-Luc university clinic[in French]. Ann Readapt Med Phys.2003;46:607-614.

2. Gil R, Kremer-Merere C, Morizio P,Gouarne R. Les ataxies, avec et sansvertige. In: Rééducation des troublesde l’équilibre. Frison-Roche, Paris;1991:72-81.

3. Schneider D, Hahn A, Claussen CF.Cranio-corpo-graphy. A neurootologi-cal screening test. Acta Oto-rhinolaryngol Belg. 1991;45:393-397.

4. Claussen CF, Schneider D,Marcondes LG, Patil NP. A computeranalysis of typical CCG patterns in1,021 neuro-otological patients. ActaOtolaryngol Suppl. 1989;468:235-238.

5. Brandt T, Dieterich M. Posturalimbalance in peripheral and centralvestibular disorders. In: Bronstein A,Brandt T, Woollacott M, eds. Clinicaldisorders of balance, posture andgait. Edward Arnold, London;1996:131-146.

6. Fukuda T. The stepping test: twophases of the labyrinthine reflex. ActaOtolaryngol. 1959;50:95-108.

7. Jaïs L, Weber B. La meilleure façonde piétiner. In: Dupui Ph, Montoya R,Lacour M, eds. Posture et équilibre.Physiologie, techniques, pathologies.Solal, Marseille; 2003:81-90.

8. Weber B, Gagey PM, Noto R. Doesrepetition change the performance ofFukuda’s test [in French]? Agresso-logie. 1984;25:1311-1314.

9. Kuipers-Upmeijer J, Oosterhuis HJ.Unterberger’s test not useful in testingof vestibular function [in Dutch]. NedTijdschr Geneeskd. 1994;138:136-139.

10. Bonanni M, Newton R. Test-retestreliability of the Fukuda SteppingTest. Physiother Res Int. 1998;3:58-68.

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11. Hickey SA, Ford GR, Buckley JG,Fitzgerald O’connor AF. Unterbergerstepping test: a useful indicator ofperipheral vestibular dysfunction?J Laryngol Otol. 1990;104:599-602.

12. Reiss M, Reiss G. Further aspects ofthe asymmetry of the stepping test.Percept Mot Skills. 1997;85:1344-1346.

13. Fregly AR, Graybiel A. An ataxia testbattery not requiring rails. AerospMed. 1968;39:277-282.

14. Shumway-Cook A, Woollacott M.Motor Control Theory and applica-tions, Williams & Wilkins, Baltimore;1995:323-324.

15. Whitney SL, Hudak MT,Marchetti GM. The dynamic gaitindex related to self-reported fall his-tory in individuals with vestibulardysfunction. J Vestib Res. 2000;10:99-105.

16. Hall CD, Schubert MC, Herdman SJ.Prediction of fall risk reduction as

measured by dynamic gait index inindividuals with unilateral vestibularhypofunction. Otol Neurotol.2004;25:746-151.

Dr. Stéphane DejardinClinique Saint-LucRue Saint Luc 8B-5004 Bouge, BelgiumE-mail: stdejardin@skynet.be