In 1985, the Royal Belgian Society for Ear, Nose,Throat, Head and Neck Surgery and the BelgianProfessional Union of Ear, Nose, Throat, Head andNeck Surgery founded the Otoneurological andExpertise Commission.

Professor R. Boniver has been the president since.At present, the members of the commission are

Professors Christian Desloovere, Nama Deggouj,Floris Wuyts and Doctors Sarah Casteleyn,Stphane Dejardin, Anne Englebert, ChantalGilain, Catherine Hennaux, Christian Van Nechel.

In 1986, the publication in the Acta Oto-Rhino-Laryngologica Belgica of expert recommendationsfor ear, nose and throat specialists introduced thetopic of vestibular exploration.

In the absence of evidence-based medicine forthis specific subject and with the encouragement of

Doctor Robillard, the commission started inDecember 2003 to draft guidelines for the explo-ration and treatment of vertigo and dizziness. Theirrecommendations are based both on the experienceof the members of the commission and on scientificadvances relating to vertigo and dizziness.

This supplement contains specialist articlesdescribing tests and examination approaches.Asterisks refer to annexes.

The guidelines are based on more recent oto-neurological findings and will be updated in thefuture.

References in the annex will give readers theopportunity to explore this subject in greater depth.

We hope this paper will bring you fruitful andenjoyable reading.

Introduction

1. Patient history

1.1. Vertigo or dizziness Description (rotatory vertigo, horizontal or verti-

cal linear sensations, postural imbalance) Start, duration, frequency Provocative event (e.g. position, orthostatism,

spontaneous, Valsalva, Tullio ) Initial manifestations Autonomic symptoms Gait: quality and perturbation factors Direction of body tilt or imbalance (lateral, pos-

terior) Falls: circumstances (current occupations, situa-

tion)1.1.1. Visual influence

Mobile environment intolerance Acrophobia 1.1.2. Agoraphobia, Anxiety (HAD and PHQ

scale in annex)1.1.3. Effect on life quality evaluation (DHI

scale in annex)

1.2. Otological symptoms (for each symptom,check laterality and temporality with verti-go)

1.2.1. Hypoacousia or hyperacousia, fluctuatinghearing, diplacousia, distorsion

1.2.2. Tinnitus: continuous, pulsating, positional

1.2.3. Hearing fullness or pressure

1.2.4. Otalgia

1.2.5. Otorrhea

1.3. Visual manifestations1.3.1. Amaurosis

1.3.2. Horizontal or vertical diplopia1.3.3. Oscillosia

1.3.4. Visual field inversion

1.3.5. Refraction correction related

1.4. Neurological manifestations (precise tempo-rality with vertigo)

1.4.1. Migraines, headache and facial pain1.4.2. Sensitive and motors manifestations (e.g.

precision in movement of upper limbs)1.4.3. Symptoms related to other cranial nerve

disorders1.4.4. Symptoms related to cervical spine disor-

ders (e.g. cervicalgia)

1.5. Prior history1.5.1. Hereditary (according to current patholo-

gy study)1.5.2. ENT1.5.3. Neurological1.5.4. Traumatic1.5.5. Cardiovascular and vascular risk factors

(hypertension, diabetes, cholesterol, smo-king)

1.5.6. Metabolic and hormonal1.5.7. Infectious1.5.8. Immunological1.5.9. Locomotor (rheumatological, orthopedic)1.5.10. Strabismus, amblyopia, multifocal refrac-

ted lenses1.5.11. Gait habits (lack of activity, chronic lying

position ...), sport (diving ...)1.5.12. Occupation1.5.13. Toxic (drugs, professional, alcohol, smo-

king)

1.6. Treatment Current, recent modification Prior (ototoxic)

Guidelines on vertigo and dizziness

4 Guidelines

Physiotherapy, cervical manipulation, vestibulartraining or repositioning manoeuvres (furtherdetails required)

2. Clinical examination

2.1. Otorhinological2.1.1. Otomicroscopic examination

2.1.2. Rhinological examination depending onsymptoms

2.2. Oculomotor and nystagmus2.2.1. Visual control test

2.2.1.1. Gaze holding ability2.2.1.2. Vertical or horizontal ocular misalignment2.2.1.3. Restriction in ocular amplitude move-

ments2.2.1.4. Smooth pursuit and saccade testing2.2.1.5. Inhibitory testing of vestibulo-ocular

reflex (VOR)2.2.2. Halmagyi test

2.2.3. With videoscopic or Frenzel glasses(without fixation)

2.2.3.1. Spontaneous and other gaze holdingabnormalities

2.2.3.1.1. Vestibular nystagmus2.2.3.1.2. Non-vestibular nystagmus2.2.3.2. Positioning nystagmus (to be conducted at

the end of the clinical evaluation)2.2.3.2.1. Methodology (patient sitting, head to

knees, supine, 90 lateral rotation of thewhole body and head to the right, andthen to the left, supine + head rotating,Hallpike or Brandt and Daroff, Rose,not necessarily in this order)

2.2.3.2.2. Clinical significance (diagnostic crite-ria)

2.2.3.3. Horizontal and vertical head shaking test2.2.3.4. Dynamic visual ability

2.3. Other cranial nerves Face sensitivity defect (if neurinoma is suspected,

complete facial sensitivity exploration, frontpain sensitivity and corneal reflex included)

Claude Bernard Horners sign Face and oropharyngolaryngeal sensitivity

2.4. Limbs2.4.1. Cerebellar signs in upper limbs (dysme-

tria, adiadocokinesia)2.4.2. Sensation or motor defect in lower limbs

2.5. Stato-kinetic tests2.5.1. Index test, finger pointing test2.5.2. Rombergs test (standard or enhanced)2.5.3. Unterberger or Fukuda2.5.4. Standard gait and star gait tests2.5.5. Gait exploration2.5.6. Dynamic Gait Index

3. Diagnostic Progression

3.1. Isolated Vertigo 3.1.1. Isolated positioning vertigo3.1.1.1. Positioning vertigo: 1st episode3.1.1.1.1. If history evocative of benign paroxys-

mal positioning vertigo (BPPV):otomicroscopy and hearing test;search for the pathological canal;execution of the repositioningmanoeuvre.

After one week, check:If asymptomatic: end of investigationIf residual symptoms persist after 2 or3 repositioning manoeuvres: see3.1.1.1.2.

3.1.1.1.2. If history and clinical presentation aty-pical

Baseline explorations: complete clinical examina-tion (see chapter 3), hearing test, BrainstemEvoked Response Audiometry (BERA),Videonystagmography (VNG) Electronystag-mography (ENG) + oculomotricity, subjectivevisual vertical perception test (SVV), VestibularEvoked Myogenic Potentials (VEMP)3.1.1.2. Positioning vertigo: relapseBaseline exploration (seen in 3.1.1.1.2) + temporalbone scan if conductive hearing loss

Guidelines 5

3.1.2. Non-positioning isolated vertigo3.1.2.1. If baseline exploration (see 3.1.1.1.2.)

non-contributive: review patient historyand test:metabolic exploration (glycaemia and thy-roid)cardiovascular explorationpsychological exploration (anxiety, pho-bia ...)migraine event

3.1.2.2. If baseline exploration suggests labyrin-thic pathology (see VNG or ENG criteria)Study of peripheral vestibular aetiologicalpathology:If no result: VEMP to exclude inferiorvestibular neuritis.If cardio-vascular risk: exploration

3.1.2.3. If baseline exploration identifies non-labyrinthic pathology(see VNG or ENG, BERA, oculomotricitycriterias)neurological explorationspecific neurological imaging

3.2. Vertigo and hearing signsIn any case, baseline exploration: hearing test, fis-tula test, BERA, VNG or ENG + oculomotricity,VVS, VEMP

3.2.1. Conductive hearing losstympanometry + acoustic reflextemporal bone TDM if otosclerosis sus-pected, aqueduct dilatation, superior canaldehiscence syndrome ...

3.2.2. Perceptive hearing losstympanometry + acoustic reflex (level ofreflex, reflex Decay test RDT)supraliminar testotoacoustic emissionstemporal bone and pontocerebellar angleMRI if retro-cochlear lesions suspected (ECOG if Mnires disease is suspected)genetic investigation if familial history(DFNA9)

3.3. Vertigo and neurological symptoms3.3.1. Vertigo and headache or facial algia

3.3.1.1. Patient with unusual vertigo and brutalheadache= Emergency (unusual intensity and loca-lisation)Exploration should be conducted withinhours.

3.3.1.1.1. Latero-cervical painLook for vertebral dissection (MRI)

3.3.1.1.2. Occipital painLook for:

expansive lesion of posterior fossa (infratentori-al tumor, blood collection ...) (TDM)

Arnold-Chiari decompensation (MRI) basilar aneurism (TDM)3.3.1.2. Vertigo and usual known headache3.3.1.2.1. Vestibular migraine

personal and familial historyusual provocative events like migraines

3.3.1.2.2. Anxious tension headache and vertigocervicalgia, whiplashimbalance without vertigo

3.3.2. Vertigo, imbalance and visuals symptoms3.3.2.1. Ocular disalignment or diplopia3.3.2.1.1. horizontal3.3.2.1.1.1. convergent nuclear or post nuclear VI nerve lesion somewhere near vestibular nuclei orbital trauma convergent spasm (post-traumatic)3.3.2.1.1.2. divergent mesencephalic lesion or nerve III orbital lesion3.3.2.1.2. vertical3.3.2.1.2.1. skew, ocular tilt reaction

vertical saccades palsy in sub-thala-mic lesions near otolithic pathway

3.3.2.1.2.2. nerve IV lesion (post-traumatic in30%)

3.3.2.2. Non-vestibular nystagmus and oscillopsia gaze-evoked nystagmus acquired pendular nystagmus flutter, opsoclonus congenital nystagmus (idiopathic, latent non-

compensated) oculomotor palsy (loss of vestibulo-ocular gain)3.3.2.3. Excessive visual dependence

(generally after vestibular deficiency)

6 Guidelines

3.3.2.4. Post-refraction change multifocal lenses major and recent refraction correction

3.4. Other vertigo3.4.1. Child vertigoAs adult specifications but particular focus on: serous otitis familial history of migraine tumours are more frequent food familial stress BPPV less frequent before 10 years of age

3.5. Imbalance without vertigo3.5.1. Imbalance with or without hearing loss,

without any neurological sign3.5.1.1. Drug side-effect or interference (local or

general), ototoxicity3.5.1.2. Haemodynamic disorders blood pressure arrhythmia3.5.1.3. Metabolic disorders diabetes dysthyroidia suprarenal dysfunction 3.5.1.4. Genetic (DFNA9 COCH gene ...)3.5.1.5. Anxiety, agoraphobia3.5.2. Combine with neurological defect

Neurological exploration must be conduc-ted

4. Laboratory examination(in accordance with 4 Diagnostic criteriaindications)

4.1. Hearing testTonal, vocal, supraliminar, depending onpathology

4.2. Tympanomatry/ Stapedial (acoustic) reflex

4.3. Auditory brainstem response

4.4. Electrocochleography (if Mnires diseaseor perilymph fistula suspected)

4.5. Otoacoustic emissions

4.6. Vestibular evoked myogenic potentials(VEMP)

4.7. VNG or ENG (normative data)4.7.1. Gaze holding in primary and lateral posi-

tions under fixation (20 to 30 maximum)4.7.2. Exploration for spontaneous and positio-

nal nystagmus without fixation

4.7.3. Ocular pursuit

4.7.4. Saccade analysis4.7.5. Optokinetic pursuit4.7.6. Rotatory/pendular tests4.7.7. Caloric test

4.8. Vertical or horizontal visual perception test

4.9. Posturography4.9.1. Static4.9.2. Dynamic

4.10. Vibratory nystagmus

4.11. Otolithic linear and rotatory test4.11.1. Excentric rotation test

4.11.2. OVAR

5. Treatment Strategy

5.1. Medical treatment

5.2. Vestibular rehabilitation: soon in B-ENT(Symposium in November 2005)

5.3. Psychological approach5.3.1. Anxiolytic5.3.2. Relaxation5.3.3. Behavioural5.3.4. Psychotherapy

5.4. Surgical treatment

Guidelines 7

Further readings

Brandt T. Vertigo. Its Multisensory Syndromes. 2nd ed.Springer Verlag, London; 1999.

Leigh RJ, Zee DS. The Neurology of Eye Movement. 3rd ed.Oxford University Press, New York; 1999.

Balow RW, Honrubia V. Clinical Neurophysiology of the Vesti-bular System. 3rd ed. Oxford University Press, Oxford;2001.

Luxon L. Text book of Audiological Medicine. Clinical Aspectsof Hearing and Balance. Martin Dunitz, London; 2003.

Brandt T, Strupp M. General vestibular testing. ClinNeurophysiol. 2005;116:406-426.

Fife TD, Tusa RJ, Furman JM, et al. Assessment: vestibulartesting techniques in adults and children: report of the

Therapeutics and Technology Assessment Subcommittee ofthe American Academy of Neurology. Neurology. 2000;55:1431-1441.

Socit Belge dOto-Rhino-Laryngologie et de ChirurgieCervico-Faciale, Groupement Belge des spcialistes Oto-Rhino-Laryngologie et de Chirurgie Cervico-Faciale.Expertise mdicale en oto-rhino-larynogologie. Recom-mandations. Acta Otorhinolaryngol Belg. 1986;40:907-915.

Vertiges chez lAdulte: Stratgies diagnostiques. Place de larducation vestibulaire. ANAES. Srie des rfrencesmdicales septembre 1997. Available at: http://www.sfmu.org/documents/consensus/rbpc_vertiges_diagn.pdf.Accessed February 1, 2008.

B-ENT, 2008, 4, Suppl. 8, 9-12

Introduction

Head-shaking nystagmus is alatent spontaneous vestibular nys-tagmus. It is provoked in a seatedpatient by rapid passive headshaking around a vertical axis.Frenzels glasses in a dark room ora video camera (videonystag-moscopy) show no spontaneousnystagmus after head shaking innormal subjects. In patients withperipheral and central vestibularlesions, however, passive headshaking is a powerful way of acti-vating spontaneous nystagmus.

Methods

HSN is elicited by encouragingvigorous, approximately sinusoidal,head shaking for 15-20 seconds.When patients stop shakingtheir heads, the nystagmus canbe observed with Frenzel lenses.Invariably, a transient (5-20 seconds) but relatively brisknystagmus is found, with the slowphases being initially directedtowards the impaired ear. Thisnystagmus is followed by a muchlonger but lower-amplitude nystag-mus with slow phases directedaway from the impaired ear.

Vertical head shaking also inducesa horizontal nystagmus but the pri-mary phase will then be directedaway from the impaired ear. Thereversal phase is small or absent.

Results

HSN has been studied for years.The most important papers wereselected from the extensive litera-ture on the subject.

In 1986, Takahashi1 studiedbiphasic HSN (b-HSN) in nine-teen patients using electronystag-mography. Sixteen of thesepatients had unilateral peripheralvestibular disturbance. As inKameis2 study, the first phasebeats towards the healthy side andthe second phase towards thedamaged side in thirteen patientsin this group (81%). In theremaining three cases (19%), thefirst phase beats towards the dam-aged side, and the second phasetowards the healthy side. Thiscontradicts Kameis findings, inwhich b-HSN was also observedin three cases of central vestibulardisturbance, indicating that b-HSN occurs not only in cases ofperipheral vestibular disturbancebut also in cases of central origin.

In 1987, Hain et al.3 used thescleral eye coil technique to studynystagmus, finding HSN in sixtysubjects with unilateral peripheralvestibular lesions.

Horizontal head shaking elicitedhorizontal nystagmus with slowphases that were initially directedtowards the side of the lesionand upwards. All subjects showeda prolonged lower-amplitudereversal phase after the initialresponse following horizontalhead shaking.

In 1989, Wei et al.4 studied108 patients referred for calorictesting and found that HSN is notas powerful a test as canal paresisfor the detection of lesions of the8th nerve.

In 1990, Takahashi et al.5 evalu-ated horizontal HSN in 85 patientscomplaining of dizziness and ver-tigo. This was done by comparingthe horizontal head-shaking testwith routine rotatory and caloricvestibular testing.

They found that HSN evokedby horizontal head-shaking is ahighly sensitive way of detectingunilateral vestibular hypofunction.Except in patients with additionalcentral vestibular imbalance or inpatients with Mnires disease,

Head-shaking nystagmus

R. Boniver

O.R.L., University of Lige, Verviers, Belgium

Key-words. Head-shaking nystagmus; vestibular dysfunction test

Abstract. Head-shaking nystagmus. Head-Shaking Nystagmus (HSN) is a latent spontaneous vestibular nystagmusprovoked by rapid passive head shaking around a vertical axis.HSN is not specific in distinguishing peripheral hypofunction from more central vestibular imbalances.This test is an excellent bedside test for detecting unilateral vestibular hypofunction but further rotatory and calorictesting will be necessary to clarify the patients condition.

10 R. Boniver

the direction of horizontal HSN ishighly significant, indicating theside of the lesion, with the fastphase beating towards the intactside. However, horizontal HSN isnot specific for distinguishingperipheral hypofunction frommore central vestibular imbal-ances. Peripheral vestibular hypo-function, as well as a centralasymmetry of the vestibularvelocity storage mechanism, caneach produce horizontal HSN,either separately or in combina-tion. So the head-shakingmanoeuvre is an excellent bedsidetest for detecting unilateralvestibular hypofunction, but fur-ther rotatory and caloric testing isstill necessary to clarify thepatients condition.

In 1991, Burgio et al.6 evaluatedHSN in 115 patients with vestibu-lar lesions. The data indicate that,with passive head movement, thehead-shaking nystagmus test isneither sensitive nor specificenough for use as a screening testfor vestibular loss.

In 1992, Hall et al.7 studied aseries of 340 patients and 20 con-trols to compare the vestibular testdata with HSN. HSN appears toreflect the underlying spontaneousnystagmus and its direction has norelationship to the side of thevestibular asymmetry.

In 1993, Fujimoto et al.8 con-ducted a prospective analysis of aseries of patients who underwent ahead-shaking test during routineENG. The incidence of head-shaking nystagmus (HSN) in adizzy population was relativelyhigh (31.7%) when comparedwith other abnormalities in theroutine ENG test battery.

Incidence rates in active andpassive head-shaking tests are alsosimilar. When present, differenttypes of HSN were identified

(monophasic (76.8%), biphasic(22.7%) and triphasic (0.5%)). Insome cases, reversals of theexpected normal patternoccurred. A high correlation wasfound between a positive head-shaking test and the presence ofspontaneous nystagmus, position-al nystagmus and caloric testabnormalities.

In 1997, Asawavichianginda etal.9 analysed a group of1300 patients with a clinical diag-nosis of peripheral vestibular dis-order. There was a positive corre-lation of HSN in patients in thepathology group compared withnormal control subjects.

In 1997, Tseng and Chao10 com-pared HSN and bithermal calorictests with ENG to determine thesensitivity of the two tests forvestibular dysfunction in 258patients. The normal limit adoptedfor canal paresis was 20%. Theseauthors found HSN to be moresensitive than canal paresis. Thesensitivity of HSN for canal pare-sis was 90%.

In 2000, Katsarkas et al.11demonstrated that the lability ofthe direction of the initial phase ofHSN is due to the reflection ofinteractions between two maintime constants associated withvelocity storage and gaze holding in the vestibular centralprocesses.

In 2002, Guidetti et al.12 exam-ined 420 patients with vestibulardiseases of different origin:peripheral, central, or both centraland peripheral. They concludedthat the sensitivity of the head-shaking test is actually poor, espe-cially over time, and that it shouldtherefore not be used alone in fol-low-up for patients with vestibulardisease.

In 2004, Iwasaki et al.13 com-pared the incidence of HSN with

the value for canal paresis (CP)obtained from a caloric test. TheHSN test is not very sensitive butis acceptable as one of the screen-ing tests for detecting asymmetricvestibular dysfunction.

In 2004, Palla et al.14 demon-strated that HSN in patients withchronic unilateral vestibulardeficit following vestibular neuri-tis is influenced by gravity.

In 2004, Perez et al.15 studiedthe characteristics of horizontalHSN and its relationship withvestibular dysfunction. Theyfound no correlation betweenHSN and clinical patterns.

Discussion

Head-shaking nystagmus (HSN)has been recognised for manyyears. It refers to the observationthat patients with vestibularlesions of either peripheral or cen-tral origin may show a transientincrease in or emergence of aspontaneous nystagmus after aperiod of vigorous head shaking.This nystagmus has traditionallybeen ascribed to the activation of alatent vestibular imbalance.

Three processes are invoked toexplain the presence and the direc-tion of the two phases of HSNaccording to Zee.16

Ewalds second law is of prima-ry importance. It states that, forhigh velocities of head rotation,excitation is a more effective stim-ulus than inhibition. This asym-metric response occurs becausevestibular afferents aresilenced/driven into inhibitorycut-off at a velocity of head rota-tion that is lower than that whichleads to saturation during excita-tion. The effect of Ewalds law ismost apparent when the head ispositioned so that the plane of theparticular semicircular canal

Head-shaking nystagmus 11

being tested is parallel to the planein which the head is rotating. Inthe case of an absent labyrinth, theincrease in peripheral vestibularactivity that is relayed centrallywith rotation towards the good ear(the excitatory direction) is greaterat high speeds of rotation than thedecrease in vestibular activity thatis relayed centrally with rotationtowards the bad ear (the inhibitorydirection). This non-linear proper-ty of the labyrinthine responseforms the basis for using high-speed rotational stimuli to detectunilateral peripheral vestibularlesions. Furthermore, to probe thefunction of a particular pair ofsemicircular canals, the headshould be positioned with theplane of the canals parallel to theplane in which the head isrotating.

With rapid head-shaking, thenon-linearity described by Ewaldssecond law leads to a continual,asymmetric increase and decreasein activity that is relayed to thecentral velocity storage mecha-nism. Consequently, there is anaccumulation of activity for slowphases directed towards theimpaired ear. When the head stopsshaking, the velocity storagemechanism gradually discharges,leading to a slowly decaying nys-tagmus with slow phases directedtowards the bad ear. To accountfor the reversal phase of HSN, wepostulate a short-term adaptivemechanism, comparable to thatwhich produces the reversal phaseof caloric or of post-rotatory nys-tagmus in normal individuals.

The combination of Ewaldssecond law, asymmetric velocitystorage and adaptation gives aplausible explanation for the pat-tern of horizontal nystagmus thatoccurs after head shaking inpatients with a unilateral peripheral

vestibular loss. Note that thishypothesis predicts that head rota-tions of low velocities should notlead to HSN, because Ewalds lawshould only become apparentwhen the speed of rotation is high.HSN caused by more centrallesions, such as asymmetries inthe velocity storage mechanismitself, might appear when thespeed of head rotation is low.Finally, if velocity storage is rela-tively ineffective, as indicated by alow VOR time constant, the pri-mary phase of HSN will be shorterand the reversal phase will emergesooner.

What is the origin of the hori-zontally directed component ofthe nystagmus induced by verticalhead shaking? The most likelyexplanation is that, in normal indi-viduals, excitation of the verticalsemicircular canals also con-tributes to the generation of hori-zontal slow phases of nystagmus.This cross-coupling betweenactivities in the vertical semicircu-lar canals and horizontal nystag-mus arises from the geometricalarrangement of the semicircularcanals within the head.

The lateral canals are pitchedupwards about 30 and the verticalcanals are tilted backwards corre-spondingly. Consequently, whenthe head is oriented in certaindirections with respect to the axisof rotation, the vertical canalscontribute to the generation ofhorizontal nystagmus and thelateral canals to the generation oftorsional nystagmus. In fact, whenthe head is pitched 60 upwards,and the body is rotated around anearth-vertical axis, a significanthorizontal component of the VOR(about 50% of that with the headupright) is still generated as itshould be even though peripheralvestibular activity with this

head orientation arises almostexclusively from the vertical semi-circular canals.

One must also remember thatexcitation of the vertical semicir-cular canals leads to ipsilaterallydirected horizontal slow phasesand that rotation around an earth-vertical axis with the head uprightleads to inhibition of activity fromthe vertical canals in the samelabyrinth in which the lateral canalis being excited. Accordingly,during vertical head shaking by apatient with only one functioninglabyrinth, activity for horizontalnystagmus accumulates in centralvelocity storage. After verticalhead shaking, there is a transienthorizontal component of nystag-mus with slow phases directedtowards the intact ear.

Conclusion

HSN is useful as a first-lineexamination in the evaluation ofdizzy patients, particularly whenother vestibular tests are impossi-ble.

It is generally admitted thatHSN is not sensitive since it iselicited in only 30-40% of patientswith a unilateral vestibulardeficit.15

HSN is also considered non-specific because the existence ofpositional HSN has beendescribed in 50% of healthy con-trol subjects, as well as in patientswithout detectable vestibularasymmetries in functional stud-ies.7,9

HSN is also found in cases ofcentral vestibular lesions.

HSN has to be interpreted withcaution, as one element amongothers in the diagnosis of vestibu-lar disease.

12 R. Boniver

References

1. Takahashi S. Clinical significance ofbiphasic head-shaking nystagmus.Auris Nasus Larynx. 1986;13 Suppl 2:S199-204.

2. Kamei T. The two-phase occurence ofhead-shaking nystagmus [in German].Arch Otorhinolaryngol. 1957;209:59-67.

3. Hain TC, Fetter M, Zee DS. Head-shaking nystagmus in patients withunilateral peripheral vestibularlesions. Am J Otolaryngol. 1987;8:36-47.

4. Wei D, Hain TC, Proctor LR. Head-shaking nystagmus: associations withcanal paresis and hearing loss. ActaOtolaryngol. 1989;108:362-367.

5. Takahashi S, Fetter M, Koenig E,Dichgans J. The clinical significanceof head-shaking nystagmus in thedizzy patient. Acta Otolaryngol.1990;109:8-14.

6. Burgio DL, Blakley BW, Myers SF.An evaluation of the head-shakingnystagmus test. Otolaryngol HeadNeck Surg. 1991;105:708-713.

7. Hall SF, Laird ME. Is head-shakingnystagmus a sign of vestibular dys-

function? J Otolaryngol. 1992;21:209-212.

8. Fujimoto M, Rutka J, Mai M. A studyinto the phenomenon of head-shakingnystagmus: its presence in a dizzypopulation. J Otolaryngol. 1993;22:376-379.

9. Asawavichianginda S, Fujimoto M,Mai M, Rutka J. Prevalence of head-shaking nystagmus in patients accord-ing their diagnostic classification in adizziness unit. J Otolaryngol. 1997;26:20-25.

10. Tseng HZ, Chao WY. Head-shakingnystagmus: a sensitive indicator ofvestibular dysfunction. Clin Otolaryn-gol Allied Sci. 1997;22:549-552.

11. Katsarkas A, Smith H, Galiana H.Head-shaking nystagmus (HSN): thetheoretical explanation and the exper-imental proof. Acta Otolaryngol.2000;120:177-181.

12. Guidetti G, Monzani D, Civiero N.Head shaking nystagmus in the fol-low-up of patients with vestibular dis-eases. Clin Otolaryngol Allied Sci.2002;27:124-128.

13. Iwasaki S, Ito K, Abbey K,Murofushi T. Prediction of canal pare-sis using head-shaking nystagmus

test. Acta Otolaryngol. 2004;124:803-806.

14. Palla A, Marti S, Straumann D. Head-shaking nystagmus depends on gravi-ty. J Assoc Res Otolaryngol. 2005;6:1-8.

15. Prez P, Llorente J.L, Gmez J.R, DelCampo A, Lpez A, Surez C.Functional significance of peripheralhead-shaking nystagmus. Laryngo-scope. 2004;114:1078-1084.

16. Zee DS. New Concepts of VestibularNystagmus in Vestibular Disorders.In: Barber HO, Sharpe JA, eds.Vestibular disorders. Year BookMedical Publishers, Chicago;1988:189-200.

Prof. R. BoniverO.R.L.University of Lige21, Rue de BruxellesB-4800 Verviers, BelgiumTel.: 087/22.17.60Fax: 087/22.46.08E-mail: r.boniver@win.be

B-ENT, 2008, 4, Suppl. 8, 13-14

Introduction

The influence of proprioceptiveneck receptors on equilibriumthrough the spinocerebellar andspinovestibular tracts has beenwell known for a long time.Hinoki et al.,1 in 1971, stressedtheir importance in dizziness dueto whiplash injury.

Vibrations at the level of neckmuscles may induce a degree ofdizziness and, in some cases, ocu-lar movements2,3 and a perturba-tion of the vertical subjective.4,5

In 1973, Lcke6 demonstratedthat vibratory stimulation of themastoid induced nystagmus inpatients with a unilateral vestibu-lar lesion.

Hamann7-9 observed that vibra-tion-induced nystagmus (VIN),usually associated with peripheralvestibular dysfunction, expresseda latent destructive nystagmusand, in 1997, he indicated theimportance of this test for thedetection of acoustic neuromas.

Halmagyi et al.10 proposed theuse of skull taps as a method ofvestibular activation.

At the present time, study of theuse of VIN is centered mainly inFrance.11,12

Physiology

In 1962, Hood13 demonstrated thatthe speed of propagation of thevibratory wave for 100 Hz fre-quency stimulation through thehead is about 100 m/sec.

Consequently, the stimulationof both labyrinths is simultaneous,

the transcranial conduction timebeing about 2 m/sec.

A unilateral vibratory stimula-tion is not specific to a unilateralvestibular stimulation.

It does not allow demonstrationof a unilateral labyrinthine weak-ness (canal paresis) but can reveala directional preponderance of thenystagmus.

It is fundamentally differentfrom the caloric test.

In 1977, Young et al.14 demon-strated in monkeys that vibratorystimulation of 125 to 350 Hz ofthe cranium modified the activa-tion of inner ear cells directlyrather than through vibration ofthe endolymph.

VIN induced by a vibratorystimulus of 100 Hz relates to a fre-quential zone of stimulation com-pletely different from the physio-logical stimulation of the rotationof the head, which corresponds tofrequencies of 0.05 to 5 Hz.

Method

The method of Dumas et al.11 isproposed:

stimulator generating vibrationsat 100 Hz with an amplitude of 0.2 mm

subject in sitting position three positions for the vibra-

tion: vertex, left and right mas-toid processes.

Results

To be considered pathological, theVIN must be identical in at least

two positions and sustained. Thenystagmus is called apreed.

To be considered abnormal, theslow phase of the VIN must bemore than 2.9/sec.

In the case of nystagmus existingprior to the vibratory stimulation,the slow phase must be signifi-cantly enhanced or decreased.

The response to the stimulusappears immediately at the begin-ning of the stimulation and stopswhen it ceases.

There is no fatigability in theresponse.

The rotatory phase is constant.Vibratory stimulation does not

induce vertigo.In 2004, Magnusson et al.15

demonstrated that EMG responsesin the lower leg were evoked byvibratory stimulation of the poste-rior neck muscles and not throughmastoid vibrations.

Dumas et al.,11 Ulmer et al.,12Ohki et al.16 observe that VIN isinconstant in peripheral laby-rinthine lesions. In these cases,when VIN is present, its directionis towards the normal labyrinth.

VIN is also found in centraldiseases such as cerebrovascularaccidents, Arnold-Chiari mal-formation or spinocerebellardegeneration.

Vibratory stimulation does notmodify the results of repositioningmanoeuvres in cases of benignparoxysmal vertigo.17

Conclusion

VIN permits the demonstration ofvestibular asymmetry in a simple

Vibration-induced nystagmus

R. Boniver

O.R.L., University of Lige, Verviers, Belgium

14 R. Boniver

way in patients whose physicalstate is incompatible with othermeans of vestibular exploration.

The vibratory test does not dif-ferentiate between central andperipheral lesions, nor does itindicate the side affected.

References

1. Hinoki M, Hine S, Tada Y.Neurootological studies on vertigodue to whiplash injury. EquilibrationRes (Tokyo). 1971;suppl 1:6-29.

2. Strupp M, Arbusow V, Dieterich M,Sautier W, Brandt T. Perceptual andoculomotor effects of neck musclevibration in vestibular neuritis.Ipsilateral somatosensory substitutionof vestibular function. Brain. 1998;121:677-685.

3. Ohyama Y. The influence of dorsalneck proprioceptive inputs on vestibu-lar compensation by three-dimen-sional analysis of neck-induced nys-tagmus [in Japanese]. NipponJibiinkoka Gakkai Kaiho. 1999;102:50-57.

4. Karlberg M, Aw ST, Halmagyi GM,Black RA. Vibration-induced shift ofthe subjective visual horizontal: a signof unilateral vestibular deficit. ArchOtolaryngol Head Neck Surg. 2002;128:21-27.

5. Karlberg M, Aw ST, Black RA, ToddMJ, MacDougall HG, Halmagyi GM.Vibration-induced ocular torsion and

nystagmus after unilateral vestibulardeafferentation. Brain, 2003;126:956-964.

6. Lcke K. A vibratory stimulus of100 Hz for provoking pathologicalnystagmus (authors transl) [inGerman]. Z Laryngol Rhinol Otol.1973;52:716-720.

7. Hamann K. Le nystagmus de vibra-tion, un signe de perturbation vestibu-laire priphrique. In: Compte rendudes sances de la Socit dOto-neurologie de langue franaise,XXVIIe Symposium. Ipsen, San Remo;1993:80-85.

8. Hamann KF, Schuster EM. Vibration-induced nystagmus A sign of uni-lateral vestibular deficit. ORL J Oto-rhinolaryngol Relat Spec. 1999;61:74-79.

9. Hamann KF. Le nystagmus de vibra-tion vis--vis du neurinome de la-coustique. In: XXXIme Symposiuminternational dOtoneurologie 1997Lige. Compte-rendu des Sances.Ipsen, Paris; 1997:100-102.

10. Halmagyi GM, Yavor RA,Colebatch JG. Tapping the head acti-vates the vestibular system: a new usefor the clinical reflex hammer.Neurology. 1995;45:1927-1929.

11. Dumas G, Lavieille JP, Schmerber S,Sauvage JP. Le test vibratoire osseuxcrnien. Rev SFORL. 2004;82:8-14.

12. Ulmer E, Chays A, Brmond G.Vibration-induced nystagmus: mecha-nism and clinical interest[in French].Ann Otolaryngo. Chir Cervicofac.2004;121:95-103.

13. Hood JD. Bone conduction: a reviewof the present position with especialreference to the contributions ofDr Georg Von Bekesy. J Acoust SocAm. 1962;32:1325-1332.

14. Young ED, Fernndez C,Goldberg JM. Responses of squirrelmonkey vestibular neurons to audio-frequency sound and head vibration.Acta Otolaryngol. 1977;84:352-360.

15. Magnusson M, Andersson G,Martensson A, Fransson P,Karlberg M, Gomez S. Vibration tothe posterior neck evokes fast EMGresponses of the lower leg, but mas-toid vibration does not. J Vestib Res.2004;67,158.

16. Ohki M, Murofushi T, Nakahara H,Sugasawa K. Vibration-inducednystagmus in patients with vestibulardisorders. Otolaryngol Head NeckSurg. 2003;129:255-258.

17. Macias JD, Ellensohn A,Massingale S, Gerkin R. Vibrationwith the canalith repositioningmaneuver: a prospective randomizedstudy to determine efficacy. Laryn-goscope. 2004;114:1011-1014.

Prof. R. BoniverO.R.L.University of Lige21, Rue de BruxellesB-4800 Verviers, BelgiumTel.: 087/22.17.60Fax: 087/22.46.08E-mail: r.boniver@win.be

B-ENT, 2008, 4, Suppl. 8, 15-22

1. Skew deviation and verticaldiplopia of vestibular origin

A vertical diplopia (one imageabove the other) may be the con-sequence of a lesion in thevestibular system, including alesion restricted to the labyrinth.The otolithic system contributes tothe control of vertical eye move-ments and alignment. In mammalswith lateral vision, a head tiltinduces an upper movement of theipsilateral eye and a lowering ofthe contralateral eye. The modifi-cation of eye-muscle implantationassociated with the shift to frontalvision added a torsional (ocularrotation around the visual axis)action to the vertical muscles. So ahead tilt in humans induces a tor-sional movement of both eyeswith an amplitude of a fewdegrees, the counter-rollingreflex. Normally, this reflex doesnot result in any vertical misalign-ment between the eyes because ofaccurate balance in the antagonistvertical eye muscles. A dysfunc-tion in any structure associatedwith this otolithic reflex, from the

labyrinth to the eye muscles,through the vestibular nuclei andthe mesencephalic nuclei of Cajal,can provoke a vertical misalign-ment with torsion of the eyes andvertical diplopia if the patient hasbinocular vision. This verticalmisalignment with torsion of theeyes consecutive to a lesion of thevestibular system is called skewdeviation. The lower eye isipsilateral to a labyrinthic orvestibular nucleus lesion, andcontralateral to a lesion locatedhigher on the otolithic pathways.The impairment of the otolithicsystem means that this skew devi-ation is often combined with aspontaneous head tilt, body latero-deviation and an error in the esti-mation of the visual vertical. Thiscomplete otolithic syndrome iscalled Ocular Tilt Reaction(OTR).1

Horizontal diplopia is never aconsequence of a direct lesion ofthe vestibular system. However, itcan result from impaired struc-tures very close to the vestibularpathways and so contribute to thelocalisation diagnosis.

Let us remember that an ocularmisalignment does not necessarilyimply diplopia. Monocular ambly-opia, alternating fixation or, para-doxically, a significant anglebetween the ocular axes caneliminate the diplopia. A contro-lateral head tilt with a normalcounter-rolling reflex can alsosometimes counteract verticaldiplopia.

There are two simple ways ofdetecting ocular misalignment.The first one consists of observingthe reflection of a lamp in bothpupils. The position of this reflec-tion should remain relatively sta-ble during gaze deviations. Thesecond consists of placing acoloured filter in front of one ofthe patients eyes. To exclude aneye misalignment, we check thatthe patient does not see twodifferent points in binocular vision,while one point is indeed seen whenwe hide each eye. This last methodcan lead to some false positiveresults when there is phoria or alack of binocular fusion. These twotechniques will allow for the easydetection of a vertical diplopia.

Neuro-ophthalmological symptoms in vertigo and dizziness

C. Van NechelNeuro-ophthalmological Unit, Erasmus University Hospital, BrusselsNeurological Department, Brugmann University Hospital, Brussels.I.R.O.N., Paris

Key-words. Dizziness; vertigo; vestibular function tests; nystagmus; diplopia

Abstract. Neuro-ophthalmological symptoms in vertigo and dizziness. The vestibular and visual systems are closelylinked in the genesis of vertigo and dizziness. An examination of these two systems is helpful in the search for anaetiological diagnosis. In ENT, this double approach can also help to avoid certain ophthalmological pitfalls such as themistaken idea that a squint cannot be of vestibular origin, that the absence of diplopia symptoms is enough to excludeany recent oculomotor paresis, or even that eyelid asymmetry is not relevant to diagnosing dizziness.This paper is intended to help in understanding the neuro-ophthalmological aspects of the guidelines. It is sometimeslimited to defining certain terms. However, on the whole, it covers diagnostic procedures.

16 Van Nechel

2. Nystagmus

This paper will not provide detailsabout the most likely localisationsdepending on the manifestationsof all the different types of nystag-mus. Several syntheses of thecontribution of nystagmus tothis localisation diagnosis areavailable.2,3 From the physiopatho-logical point of view, it should beremembered that, although thereare three mechanisms responsiblefor nystagmus, only the first is ofvestibular origin.

a) Nystagmus associated withimpaired vestibulo-ocularreflexThese deficits are characterisedby both eyes being pulled inone direction, with this move-ment corresponding to the slowphase of the nystagmus. Thisdirection depends directly onthe site of the lesion. The planeorientations of the semicircularcanals are close to those of theoculomotor muscles. Eachcanal has a privileged relationwith the muscle that moves theeye in a direction opposite tothe head movement stimulatingthat canal. Ocular muscleimplantation precludes a pure-ly vertical eye movementthrough the stimulation of asingle vertical muscle. Themovement will always bearound a vertical axis associatedwith a torsional movement ofthe eyeball. It is reasonableto assume that this associationexcludes the possibility of nys-tagmus with a purely verticalor rotatory slow phase causedby a unilateral peripherallesion. At the central level it isnecessary to keep clearly inmind that the conjugate hori-zontal eye movements are, in

essence, organised at the levelof the pons. It is at this levelthat we find the abducensnucleus (VI), the starting pointfor the stimulation of thelateral rectus muscle and theascending pathway (mediallongitudinal fasciculus) whichstimulates the motoneurons ofthe medial rectus muscle at thelevel of the common oculomo-tor nucleus. Oculomotor nucleiresponsible for vertical and tor-sional eye movements arelocated higher in the brain-stem, at the level of the mid-brain. As a result, nystagmus ofcentral origin associated with alesion situated at the brainsteminput level in the vestibularpathways (ponto-medularlevel) will be horizontal or less frequently vertical,whereas a lesion at the mesen-cephalic level will usuallyresult in vertical, torsional and rarely horizontal binocularnystagmus.

b) Nystagmus resulting frominability to maintain one orboth eyes in an eccentric posi-tionHere, elastic elements try toreturn the eye to the primaryposition, resulting in the slowphase of the nystagmus, whichwill therefore change directionaccording to the position ofeyes. Accordingly, there willbe right horizontal nystagmuswhen looking to the right, leftnystagmus in left gaze, up-beatnystagmus when looking up,and down-beat nystagmus inthe reverse gaze direction. The inability to maintain oneor both eyes in an eccentricposition can result from a mus-cular paresis or a weaknessof the neurological structures

commanding ocular muscles.When a nystagmus of this kindis binocular and conjugate, it isgenerally caused by a failure ofthe integrator of the horizontaland vertical eye movementsand always corresponds to acentral lesion. However, itshould be kept in mind that thefirst cause of this failure isassociated with medication(psychotropic, anti-epileptic).

c) Nystagmus caused by visuo-motor-loop impairmentEye fixation and pursuit resultfrom the permanent correctionof the position of the eyes tocompensate for retinal slip. Achange in the associated feed-back loops can induce ocularoscillation or drift. The impair-ment of these loops can affectboth perception and motor ele-ments. This group includescongenital nystagmus,acquired pendular nystagmusand non-nystagmic eye fixa-tion instabilities (square wavesand ocular flutter, opsoclonus).

3. Vestibulo-ocular inhibition

This is usually evaluated withelectro-nystagmography or videonystagmography but it can be alsoclinically tested by asking patientsto stretch out their arms in front ofthem and to look at their thumbswhile rotating the head and thearms together. Any inability tomaintain the gaze on the thumbs iseasily detected by the appearanceof a nystagmus during the rota-tion. The diagnosis of a deficit inthe inhibition of the vestibulo-ocular reflex is not always correct.It should be remembered that thisimmediate inhibition results fromthe genesis of another eye move-ment in the opposing direction but

Neuro-ophthalmological symptoms in vertigo and dizziness 17

at a speed identical to the slowphase of the vestibulo-ocular nys-tagmus.3 At the speeds usuallytested, a pursuit movement can-cels the slow phase of the nystag-mus. The inhibition will thereforebe impaired if the pursuit systemis failing. A central lesion couldvery well spare this system of eyepursuit. The correct interpretationis therefore that a deficit investibulo-ocular reflex inhibitionsignals a central lesion but theopposite is not necessarily true.The preservation of normal inhibi-tion does not indicate that thedeficit is of labyrinthic origin.

4. Tilt of the visual fields (roomtilt illusion)

Patients perceive a rotation, oftenof 90 or 180 degrees, of the visualfields with both eyes. This rotationcan occur in the three spatialplanes. They are usually brief andfound most commonly in brain-stem4 or cerebellar infarcts, in cor-tical lesions more particularlyduring vestibular epilepsies butalso in peripheral lesions.5 Theyare a consequence of the faultyintegration of visual and otolithicinformation. This visual tilt israrely present simultaneously withabnormalities of the subjectivevisual vertical line because the lat-ter is of otolithic origin and can becorrected by adequate visualinformation.

5. Visual symptoms associatedwith an improvement in visualrefraction

Vision contributes to balancethrough two mechanisms. Firstlythrough the analysis of the contentof the visual fields, by extractingvertical or horizontal referencesand anticipating destabilisation

factors (obstacles, escalators).And secondly by allowing sub-jects to estimate their own stabili-ty. This is done by analysing themovement of the projections onthe retina of fixed visual targets,or by measuring the eye move-ments necessary to stabilise thisprojection on the retina. All thefactors that may interfere with themovement of the projection offixed visual targets on the retinamay therefore affect the ability ofsubjects to estimate their stabilityon the basis of visual information. The most common disruptive ele-ments include the prismatic effectof lenses, any drastic modificationof refraction, for example after cata-ract surgery, or ocular instabilitiesassociated with abnormal eyemovements.

Multifocal lenses merit particu-lar attention. The correction theybring about changes with the ver-tical direction of the gaze. Theprismatic effect, in other words thedeviation of light rays caused bythe curvature of the glasses, alsovaries according to the verticalposition of the eyes. This modifiesthe amplitude of the compen-satory eye movement for a headmovement (vestibulo-ocular gain)as a function of the vertical posi-tion of the eyes. In other words,the same 10-degree movement ofa visual target will require the eyeto turn more than 10 degrees whenfocusing for close vision, and lessthan 10 degrees when focusing forremote vision. The stabilisation ofthe visual environment and theestimation of subject stabilityfrom fixed visual targets thereforebecomes much more complexbecause the analysis has to changefor every vertical position of theeyes. Although a lot of subjectsquickly adapt, others never do.

Similarly, when there is a dras-

tic correction in astigmatism,there may be interference withspace perception and particularlyof the orientation of vertical orhorizontal lines.

If subjects can estimate theirown stability by analysing the eyemovements required to stabilisethe image on the retina, it is clearthat any paresis of an ocular mus-cle or any modification in eyemotility may induce vertigo symp-toms.

6. Ocular saccade impairments

Two types of ocular saccadeabnormalities are particularly sig-nificant for dizziness: saccadehypermetria and the slowing ofthe vertical saccades.

a) Saccade hypermetriaSaccades are fast and precisemovements. These two charac-teristics make them particular-ly sensitive to dysfunction inseveral structures of the brain-stem. In particular, lesions inthe cerebellar system willimpair the precision and some-times also the speed of the sac-cades. This loss of saccade pre-cision will appear as saccadeamplitudes that are either tooweak (hypometric) or toostrong (hypermetric). Althoughdysfunctions in many struc-tures involved in saccade pro-gramming can producehypometria, saccade hyperme-tria is almost specific to lesionsof the cerebellar vermis. Othermedian cerebellar structurescontrol vestibulo-ocular reflexgain and play an essential rolein balance. Hypermetric sac-cades against a background ofvertigo or dizziness are there-fore strongly suggestive of thepresence of a cerebellar

18 Van Nechel

syndrome. For mechanical rea-sons associated with the orbit,the probability of detectinghypermetric saccades is dou-bled when we test the precisionof centripetal saccades, inother words when the gazemoves from an eccentric posi-tion, returning to the primaryposition. Clinical diagnosisinvolves asking patients to tar-get alternately one finger situ-ated between 20 and30 degrees laterally and thesecond situated in front ofthem. The clinician will lookfor the eyes overshooting eachtarget, followed by a correctivesaccade. These hypermetricmovements are easily recog-nisable on saccade recordingsin so far as the saccades areunpredictable in terms ofamplitude and position, pre-venting the progressiveimprovement of precision byanticipating saccades with thesame amplitude.

b) Slowing of vertical saccadesA vestibular otolithic syn-drome is frequently the conse-quence of an ischaemic lesionin the terminal territory ofbrainstem arteries. The lesionis situated in the sub-thalamicregion, and extends up to themidbrain. This mesencephalicextension is responsible for theotolithic syndrome, which isoften associated with a slowingof the vertical saccades, with-out any abnormality in hori-zontal saccades. The pre-nuclear structures specificallyinvolved in the realisation ofvertical saccades (mesen-cephalic reticular formationand, in particular, the rostralinterstitial nucleus of the medi-an longitudinal fasciculus) are

near the otolithic afferences ofoculomotor nuclei. When thevertical eye misalignmentrelated to the otolithic deficitis clear in the acute phase, theslowing of the vertical saccadesmay be the only remainingsign several months afterthe sub-thalamic lesion. Thisdeficit is easily highlighted bysimply asking the patient toswitch as quickly as possiblebetween two targets (for exam-ple the index fingers of theexaminer) located one abovethe other.

7. The subjective visual vertical

The subjective visual vertical(SVV) of a subject is the anglebetween the physical vertical line(gravitational axis) and the posi-tion of a visual linear mark adjustedvertically by the subject. ThisSVV is probably built up on thebasis of sensory vestibular, visualand proprioceptive informationwhich include abdominal sensors.Other perceptions such as thedynamic moments of inertia mayalso contribute. The subjectivevisual vertical is not an indicatorof the postural vertical (the bodyaxis when a subject thinks he/sheis vertical), because the impor-tance of sensory information inthe estimation of these two verti-cal references is different. Thisexplains the discrepancies foundbetween postural deviation andthe SVV. The sensitivity of theotolithic organs to gravity sug-gests that they play an essentialrole in the estimation of thephysical vertical axis orientation.Visual information may, however,modify this perception. The effec-tive use of these otolithic and visu-al data for postural control doesindeed imply a correction relative

to the position of the head withregard to the trunk, and the differentsegments of the body in space.Cervical somaesthetic informa-tion, cutaneous, muscular andarticular data are therefore neededto estimate the orientation of thephysical vertical axis correctly.

The SVV relates only to thevisual representation of the verti-cal axis and is measured in theabsence of any visual reference. Itseems particularly dependent onthe position of the head in spaceand does not seem to be very sen-sitive to variations in the positionof the cervical column or the body[data submitted for publication].In binocular measurements, theSVV is less sensitive to eye tor-sions induced by oculomotorparesis, even though a binocularapproach can also reduce its sensi-tivity to some cases of otolithicdysfunction. With methods of thiskind, the SVV can be consideredto be an otolithic evaluation. TheSVV is frequently impaired afterlabyrinthic lesions, lesions of thevestibular nerve or vestibularpathways in the brainstem and inthe cortical vestibular areas.

The distribution of the normalvalues obtained for binocularSVV measurements with the headstraight using a glowing barmoving in rigorously controlleddarkness (Vertical Test) in 81 sub-jects shows a deviation greaterthan 2.8 in fewer than 5% ofnormal subjects.6

8. Visual dependence and visualvertigo

Vision contributes to the preserva-tion of balance, not only by allow-ing us to detect and anticipateobstacles or irregularities in theground but, in particular, by sup-plying vertical and horizontal

Neuro-ophthalmological symptoms in vertigo and dizziness 19

references which contribute to theadjustment of our perception ofthe physical vertical. Finally,movements in the projections offixed visual targets on the retina,or the eye movements needed tostabilise this projection, allow usto estimate and therefore correctour own stability. Problems arisewhen this visual strategy is used incircumstances where the availablevisual information is not appropri-ate.7 If most of the visual field isoccupied by mobile elements, or ifall fixed visual landmarks aretaken away, the subject must beable to disregard this visual infor-mation and use vestibular orsomaesthetic information more tocontrol balance. The use of visualinformation in these conditionswill not allow subjects to turn orstabilise themselves correctly inspace, and often lead to a sensa-tion of nausea as a result of theactivation of the alarm system(parabrachialis nucleus - limbiccerebral cortex system). This per-sistence in the use of inadequatevisual information can be theresult of a vestibular deficit or aloss of the ability to select an ade-quate source of sensory informa-tion. This can persist in spite of therecovery of normal vestibular func-tion, when a subject has got used tocontrolling balance with a visualstrategy. Vestibular rehabilitationcan be used in an attempt to helpthese patients regain the abilityto select adequate sensory infor-mation.

9. Dynamic visual acuity

The dynamic visual acuity (DVA)test is a method for measuring theclinical functioning of the vestibu-lo-ocular reflex. This test mea-sures visual acuity during hori-zontal sinusoidal head rotations of

at least 2 Hz and greater than120/second, which exceeds thelimits at which it is possible toprevent compensation with antici-patory slow eye movements andcatch-up saccades.

The subjects are asked to iden-tify symbols or letters on a visualacuity chart. This is continued onsuccessive lines until the subjectmisses three of the five optotypeson a line.

This is done under two condi-tions: head stationary (staticbinocular visual acuity - SVA),and with the head being passivelyrotated sinusoidally, 15 from cen-tre to the left and right, to the beatof a metronome at 2 Hz (dynamicvisual acuity - DVA).

A difference greater than twolines between SVA and DVA con-stitutes a failure score.

This test has been shown to besensitive for vestibular impair-ment in adults8 and children.9 Theresults of the study of Rine et al.9indicate that the clinical DVA testis a reliable and valid test of gazestability in children, and can beused to screen for vestibular hypo-function in children as young asthree years of age.

10. Migraine and vertigo

Vertigo has been found to occursignificantly more frequently inpatients with migraine than incontrol subjects. The internationalclassification of migraines (IHS)includes the symptom vertigoonly as an aura of a basilarmigraine. This aura has to consistof at least two of a number ofsymptoms, including: vertigo, tin-nitus, dysarthria, binocular visualsymptoms in the nasal and tempo-ral fields, hearing loss, diplopia,ataxia, bilateral paraesthesia,bilateral paresis or a decline of the

consciousness level. However,clinical practice suggests that thelink between vertigo and migraineis much more frequent, beingfound outside the group ofpatients who fulfil these criteria,and that vertiginous monosympto-matic aura is common.

Neuhauser et al.10 assess theprevalence of migrainous vertigoin patients with migraine and inpatients with vertigo according totwo different diagnoses.

The diagnosis of definitemigrainous vertigo was based onthe following criteria:

1. Episodic vestibular symptomsof at least moderate severity(rotational vertigo, other illu-sory self or object motion,positional vertigo, head motionintolerance, i.e., sensation ofimbalance or illusory self orobject motion that is provokedby head motion)

2. Migraine according to the IHScriteria

3. At least one of the followingmigrainous symptoms duringat least two vertiginous attacks:migrainous headache, photo-phobia, phonophobia, visual orother auras

4. Other causes ruled out byappropriate investigations

A separate diagnostic category ofprobable migrainous vertigo waschosen for patients who did notentirely fulfil the above criteria formigrainous vertigo but were stillconsidered to have migrainousvertigo as the most likely diagno-sis.

The diagnosis of probablemigrainous vertigo was based onthe following criteria:

1. Episodic vestibular symptomsof at least moderate severity(rotational vertigo, other

20 Van Nechel

illusory self or object motion,positional vertigo, head motionintolerance)

2. At least one of the following:migraine according to the cri-teria of the IHS; migrainoussymptoms during vertigo;migraine-specific precipitantsof vertigo, e.g., specific foods,sleep irregularities, hormonalchanges; response to anti-migrainous drugs

3. Other causes ruled out byappropriate investigations

Vestibular symptoms were definedas mild if they did not interferewith daily activities, moderateif they interfered with but didnot impede daily activities, andsevere if patients could notcontinue daily activities.

The results of this study showthat the prevalence of migraineaccording to the IHS criteria washigher in the dizziness clinic group(38%) compared with the age- andsex-matched control group (24%,p

Neuro-ophthalmological symptoms in vertigo and dizziness 21

migraine with aura at olderages

6. Other causes ruled out.Differential diagnosis:Mnires disease, vestibularepilepsy, perilymphatic fistula,posterior fossa tumours andpsychogenic disorders

11. The Claude BernardHorner syndrome

The interruption of the orthosym-pathetic eye fibres is known asClaude-Bernard-Horner syndrome(CBH). It is characterised by ipsi-lateral ptosis consecutive to thedenervation of the Mller superioreyelid muscle and also by a dis-creet rise of the lower eyelidcaused by denervation of itsretractor muscle. In addition thissyndrome includes anisocoriawith ipsilateral miosis. The aniso-coria may be moderate and notexceed 1/2-1 mm. It is clearer in

half-light. The anhydrosis of theipsilateral hemi-face present inCBH syndromes of central originis not obvious. It is often transi-tional because it is compensatedby denervation hypersensitivity tocirculating adrenergic substances.The diagnosis can be confirmedby eye-drop tests from ophthal-mologists (cocaine test followedby the hydoxy-amphetamine test).At the ponto-medullar level, theorthosympathetic fibres pass justinside the vestibular nuclei. Thereis therefore a high probability thata lesion of the vestibular nucleusis associated with CBH syndrome.Only larger lesions will resultin the classic syndrome ofWallenberg. The presence of CBHsigns can still indicate a centralorigin months after a vestibulardeficit.

In a post-traumatic context,CBH syndrome can result fromthe impairment of the orthosym-

pathetic fibres at the level of thecervical cord or in the pathwayalong the carotid arteries. Weshould also bear in mind that aCBH syndrome can result from amigraine crisis and this can alsolead to dizziness and vertigo.

12. Facial sensitivity deficit

In the brainstem, post-synapticpain sensitivity fibres of thetrigeminal nerve extend down tothe first cervical levels. They con-stitute the downward root of thetrigeminal nerve and reach theupper spinal cord. At the bulbarlevel, these fibres are situated justinside vestibular nuclei. They area part of the same vascular territo-ry as the vestibular nuclei, and areirrigated by the terminal branchesof the antero-inferior cerebellarartery. Other branches of the sameartery irrigate the internal ear. Asensory deficit of the face

Figure 2

22 Van Nechel

associated with acute dizzinessindicates the presence of a lesionat the level of the floor of thefourth ventricle, associated or notwith a labyrinthic lesion. Sincetopography is inverted in thisdownward root of the trigeminalnerve, it is mostly in the upperpart of the face that we find thesensory deficit related to such alesion.

13. Transient visual obscura-tions (Visual Eclipses)

Transient visual obscurations arebrief moments of binocular dark-ening of the vision. They arefound in 68% of patients sufferingfrom idiopathic intracranialhypertension12 but also in casesof orthostatic hypotension, andsecondary intracranial hyper-tension.

14. Oscillopsia

These are not specific and canresult from all acquired nystag-mus, decompensated congenitalnystagmus, non-nystagmic eye

oscillations, superior oblicmyokimia and spasmus nutans.

An overview of abnormal eyemovement in adults and in infantsis given in Figures 1,2.13

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5. Malis DD, Guyot JP. Room tilt illu-sion as a manifestation of peripheralvestibular disorders. Ann Otol RhinolLaryngol. 2003;112:600-605.

6. Van Nechel C, Toupet M., Bodson I.The subjective visual vertical. AdvOtorhinolaryngol. 2001;58:77-87.

7. Guerraz M, Yardley L, Bertholon P, etal. Visual vertigo: symptom assess-ment, spatial orientation and posturalcontrol. Brain. 2001;124:1646-1656.

8. Tian JR, Shubayev I, Demer JL.Dynamic visual acuity during passiveand self-generated transient head rota-tion in normal and unilaterallyvestibulopathic humans. Exp BrainRes. 2002;142:486-495.

9. Rine RM, Braswell J. A clinical testof dynamic visual acuity for children.Int J Pediatr Otorhinolaryngol. 2003;67:1195-1201.

10. Neuhauser H, Leopold M, vonBrevern M, Arnold G, Lempert T. Theinterrelations of migraine, vertigo,and migrainous vertigo. Neurology.2001;56:436-441.

11. Dieterich M, Brandt T. Episodic verti-go related to migraine (90 cases):vestibular migraine? J Neurol. 1999;246:883-892.

12. Giuseffi V, Wall M, Siegel PZ,Rojas PB. Symptoms and diseaseassociations in idiopathic intracranialhypertension (pseudotumor cerebri): acase-control study. Neurology.1991;41:239-244.

13. Van Nechel C. Nystagmus spontanset mouvements oculaires anormaux.In: GEV, ed. Vertiges 2000. Masson,Paris; 2000:3-20.

Dr. C. Van NechelService de Revalidation NeurologiqueCHU BrugmannPlace Van Gehuchten 4B-1020 Bruxelles, BelgiumE-mail: cvnechel@ulb.ac.be

B-ENT, 2008, 4, Suppl. 8, 23-25

The head impulse or head thrusttest was first described byHalmagyi and Curthoys in 1988.1It has acquired an increasinglyimportant place in the clinicalexamination of the vertigo patient.It detects severe unilateral loss ofsemicircular canal (SCC) functionclinically; it is more sensitive andspecific than the traditionalRomberg and similar tests; and itis particularly important in theemergency unit, where it can dis-tinguish between vestibular neuri-tis and cerebellar infarction,which can both generate similarsymptoms suggesting an initialattack of severe acute vertigo. Theresult of the head thrust test isdefinitely normal in a patient witha cerebellar infarction but abnor-mal in a patient with vestibularneuritis.

General physiological back-ground: the push-pull principleof the vestibulo-ocular reflex

The peripheral vestibular sensorstransmit motion to the brainthrough frequency encoding. LikeFM radios, our brains continuous-ly receive frequency modulatedsignals. A normal resting dis-charge rate of approximately90 spikes per second is modulatedsuch that any increase in this ratecorresponds to excitation and a

decrease to inhibition. Thepolarisation of the hair cells in thehorizontal semi-circular canal issuch that deflection of the stere-ocilia in the cupula towards thekinocilium (ampullo- or utricu-lopetal) results in hair cell depo-larisation and the activity of theprimary afferent neurons thereforeincreases. Deflection of the stere-ocilia away from the kinocilium(ampullo- or utriculofugal) resultsin hair cell hyperpolarisation anddecreased primary afferent neuronactivity.

The orientation of the left andright semi-circular canals in thehead is such that any movementalways induces an antagonisticresponse in both canals.Horizontal head movements in theyaw plane are an example. Duringrightward head rotation, theendolymph in the lateral semi-cir-cular canals on both sides lagsbehind, bending the cupula of theright SCC towards the vestibulum(ampullo- or utriculopetal) andsimultaneously deflecting thecupula of the left SCC away fromthe vestibulum (ampullo- orutriculofugal). A key difference isthe polarisation of the hair cells.Indeed, since the the hair cells inthe right and left canals areimplanted in opposing directions(in a mirror image fashion), thedeflection on the leading rightside induces the movement of the

stereocilia towards the kinocilium,whereas the movement of thestereocilia is away from the kino-cilium in the opposing, follow-ing ear. As a result of this push-pull principle, the activity ofright lateral SCC primary afferentneurons increases, and, at thesame time, the activity of leftlateral SCC primary neuronsdecreases with respect to the nor-mal resting discharge rate.

The activity of the lateral SCCprimary afferent neurons is modu-lated by horizontal head rotation.The firing rate increases in theleading ear (the ear towards themovement is directed) anddecreases in the following ear.This is the push-pull principle ofthe VOR.

The right medial vestibularnucleus in the brainstem receivesan increased input from the rightlateral SCC primary neurons (nocrossing). This excites the activityof type I secondary vestibular neu-rons. These excitatory neuronsdrive the leftward compensatoryeye movements of the VOR, toensure gaze stabilisation.However, commissural disinhibi-tion from the left lateral SCC pri-mary neurons also contributes tothe excitation of the type 1 neu-rons. Both excitation of the rightSCC and disinhibition of the leftSCC are therefore needed for anoptimal VOR.

Principle of the head impulse (thrust) test or Halmagyi head thrust test (HHTT)F. Wuyts

Antwerp University Research centre for Equilibrium and Aerospace (AUREA), Antwerp University Hospital, Universityof Antwerp, Antwerp, Belgium

Key-words. Vestibular test; semicircular canal; head impulse test; head thrust test

24 F. Wuyts

Head thrust test

The head thrust test is primarilybased on the fact that inhibition ofprimary and secondary vestibularneurons cannot produce fewerthan 0 spikes per second.Excitation can drive the dischargerate from 90 to 300 or more spikesper second. So when the healthyside is excited for a high accelera-tion head movement, the healthyside will generate the larger partof the VOR, since the disinhibitionof the ipsilateral type-1 neuronsby the contralateral SCC con-tributes relatively little to theVOR. Passive head impulses orthrusts should be typically rapidbut with a small amplitude( 20 degrees). Their velocityranges up to 180 deg/s but highacceleration is particularly impor-tant (3000-4000 deg/s2). Theyhave to be unpredictable since

the patient very quickly learnsto anticipate and this reducesthe sensitivity of the test to aconsiderable extent. The examinershould therefore thrust the head ofthe patient firmly from left to rightat random and from right to left alittle later, i.e., not immediately.The starting position should besuch that the patients head isturned slightly past the midline,and it should then be thrust justpast the midline to the oppositeside. Here, amplitude is low butacceleration can be considerable.This test demands some training,particularly with respect to thepositioning of the hands on theside of the head and holding thehead firmly. The instruction to thepatient is to fix on a point in thedistance behind the examiner.

When the subjects head isturned to the side of the lesion, theVOR is deficient and the eyes will

move with the head so that they nolonger fix on the point in the dis-tance. The patient therefore needsa refixation saccade just after thethrust. When the head impulse isin the direction of the healthy side,the VOR will maintain the targeton the fovea and no refixation sac-cade will be needed.

The head-thrust test is positivefor the side that causes the refix-ation saccade upon thrust(Figure 1)

It is not only the lateral SCC thatcan be examined this is, in asense, a clinical approximation ofthe caloric test but also the otherSCC. Here, the patients headmust be thrust in the RALP orLARP planes (Right Anterior Left Posterior or Left Anterior Right Posterior SCC).2

Figure 1Left: the clinician holds the head of the subject firmly and turns it briskly to the left. Centre: After the rotation to the left, the subjectmaintains the gaze on the distant fixation point, i.e., the eyes stay stable in space.Right: After abrupt rotation to her right, the subject moves her eyes with her head and loses the target. A refixation is necessary tofixate the point again (not shown). The side towards the gaze fixation is lost is the deficit side, i.e., the patients right.

Head impulse (thrust) test 25

References

1. Halmagyi GM, Curthoys IS. A clinicalsign of canal paresis. Arch Neurol.1988;45:737-739.

2. Aw ST, Fetter M, Cremer PD,Karlberg M, Halmagyi GM. Individualsemicircular canal function in superiorand inferior vestibular neuritis.Neurology. 2001;57:768-774.

Prof. Floris Wuyts Head of the Antwerp University ResearchCentre for Equilibrium and AerospaceDepartment of ENT Antwerp University Hospital University of AntwerpWilrijkstraat 10 2650 Edegem, BelgiumE-mail: floris.wuyts@ua.ac.be

B-ENT, 2008, 4, Suppl. 8, 27-28

Introduction

Tullios phenomenon (TP) is a pat-tern of sound-induced imbalancesymptoms, motor responses ofthe eyes (nystagmus), head(myogenic responses) and otherspinal neuron synkinesis (posturalsway).1,2 It may be physiologicalor pathological.

Physiological TP

Very loud sounds (250-500-1000 Hz or clicks at 110 dB)applied mono-aurally (but not bin-aurally) may elicit posturalresponses in normal subjects.1,3,4This physiological Tullios phono-menon results in postural sway,increasing with closed eyes, whenrecorded with posturographictechniques.

It also induces myogenicresponses in the sterno-cleido-mastoidian muscles, when recordedwith vestibular evoked myogenicpotential (VEMP) techniques.1,4-7Those vestibulocollic responses(provoked by a physiological TP)are thought to be useful in explor-ing saccular function.

Pathological TP

This form corresponds to avestibular hypersensitivity to sound,resulting in perceived vertigo orunsteadiness. The otolothic-likesymptoms are elicited with lessloud sounds,

28 N. Deggouj et al.

Other pathological modifica-tions may be involved in TP. Apathological contiguity of thetympano-ossicular chain andmembranous labyrinth may beassociated with it. It is observedin cases of dislocated ossicularchain, stapes hyperlaxity, fractureof the footplate or of the labyrinth,fibrotic damping of the ossicularchain, fibrosis of the inner ear,traumatic labyrinth, perilym-phatic fistula and endolymphatichydrops.1,3-14

The distance between the foot-plate and the utriculus is only0.5 mm in the posterior part ofthe oval window.11 Membranousconnections exist between theutriculus and the footplate in 25%of subjects.11 An increase inthose connections may favoursonovestibular hypersensitivity.

Diagnosis

When a subject presents symp-toms of sonovestibular hypersen-sitivity, the TP diagnosis must beconsidered. It is confirmed by dif-ferent tests like a positiveHennebert sign, sound-inducednystagmus, sound-induced posturalresponses recorded with posturo-graphic tests and falls in VEMPthresholds.

A morphological modificationof the middle and inner ear mustbe considered. Hyperlaxity maybe suspected in cases where thereis a fall in the resonance frequen-cy of the ear. A CT scan of the

temporal bone should show anysemi-circular canal dehiscence.

Conclusion

Pathological Tullios phenomenonis characterised by subjective andobjective sonovestibular symp-toms resulting from abnormalhypersensitivity to normal soundsof the vestibular end organssecondary to morphologicalchanges in vibration and pressuretransmission between the externaland the inner ear.

References

1. Russolo M. Sound-evoked posturalresponses in normal subjects. ActaOtolaryngol. 2002;122:21-27.

2. Brandt Th. Vertigo: its multisensorysyndromes. 2nd ed. Springer Edition,Berlin; 1998:14-15,106-112.

3. Teszler CB, Ben-David J, Podoshin L,Sabo E. Sonovestibular symptomsevaluated by computed dynamic pos-turography. Int Tinnitus J. 2000;6:140-153.

4. Watson SR, Halmagyi GM,Colebatch JG. Vestibular hypersensi-tivity to sound (Tullio phenomenon):structural and functional assessment.Neurology. 2000;54:722-728.

5. Sheykholeslami K, Schmerber S,Habiby Kermany M, Kaga K.Vestibular-evoked myogenic poten-tials in three patients with largevestibular aqueduct. Hear Res.2004;190:161-168.

6. Colebatch JG. Vestibular evokedpotentials. Curr Opin Neurol. 2001;14:21-26.

7. Bronstein AM, Faldon M, Rothwell J,Gresty MA, Colebatch J, Ludman H.Clinical and electrophysiological

findings in the Tullio phenomenon.Acta Otolaryngol Suppl. 1995;520:209-211.

8. Carey JP, Hirvonen TP, Hullar TE,Minor LB. Acoustic responses ofvestibular afferents in a model ofsuperior canal dehiscense. OtolNeurotol. 2004;25:345-352.

9. Tilikete C, Krolak-Salmon P, Truy E,Vighetto A. Pulse-synchronous eyeoscillations revealing bone superiorcanal dehiscence. Ann Neurol. 2004;56:556-560.

10. Suzuki M, Kitajima N, Ushio M,Shintani M, Ishibashi T. Changes inthe Tullio phomenon and the fistulasign in the course of endolymphatichydrops. ORL J OtorhinolaryngolRelat Spec. 2003;65:125-128.

11. Backous DD, Minor LB,Aboujaoude ES, Nager GT. Relation-ship of utriculus and sacculus to thestapes footplate: anatomic implica-tions for sound-and/or pressure-induced otolith activation. Ann OtolRhinol Laryngol. 1999;108:548-553.

12. Lesinski A, Kempf HG, Lenarz T.Tullio phenomenon after cochlearimplantation [in German]. HNO.1998;46:692-694.

13. Rottach KG, von Maydell RD,DiScenna AO, Zivotofsky AZ,Averbuch-Heller L, Leigh RJ.Quantitative measurements of eyemovements in a patient with Tulliophenomenon. J Vestib Res. 1996;6:255-259.

14. Brandt TH, Dieterich M. Differenttypes of skew deviation. J NeurolNeurosurg Psychiatry. 1991;54:549-550.

Pr. N. DeggoujCliniques UCL - Saint-LucENT Departmentavenue Hippocrate 10B-1200 Brussels, BelgiumE-mail: Naima.Deggouj@uclouvain.be

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:

Jendrassiks 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. DejardinClinique 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

Rombergs 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.

Rombergs 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 Dieterich5classified 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.

Tumarkins otolithic crisis: inthis particular version of Mniresdisease, 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 Horners 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 patientsinability to maintain an uprightposture.

One exception should be noted:in some cases of Wallenbergssyndrome, 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 1Normal values for the longitudinal and lateral sway as measured by craniocorpography

during Rombergs test. These data were derived from a neuro-otological data bankwith 10,335 normal and neuro-otological cases [Claussen CF: communication at the

30th 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 Fukudasstepping 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-ders 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 Fukudas 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

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. Nyabendas 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 Fukudas 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 thems