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EVALUATION OF BALANCE
BOX 5.1 ‘RED FLAGS’ FOR ACUTE BRAIN IMAGING IN ACUTE VERTIGO
• Acute unilateral deafness (AICA infarct)
• Acute (occipital) headache (posterior fossa stroke)
• Any central symptoms or signs (cranial nerves, multidirectional or vertical/
torsional nystagmus, skew eye deviation, limb numbness, weakness or ataxia)
A negative (normal) head-impulse test (the vertigo is unlikely to be peripheral)
AICA, anterior inferior cerebellar artery.
Source: Modied From Seemungal and Bronstein (2008).
Triggers are critically important for diagnosis in patients with recurrent symptoms.
Incorrectly, clinicians may believe neck movement–related dizziness indicates dubious entities like cervical vertigo, before excluding common vestibular disorders, particularly BPPV.
Tables 5.3 and 5.4 list triggers and associated symptoms.
Most patients with a single acute vertigo attack recover fully and most patients with recurrent vertigo are free of symptoms between attacks, but not all. Given vertigo’s prevalence,
the small proportion of not fully recovered patients develop chronic dizziness, contributing
signicantly to specialist clinics. Chronic dizziness may result from many factors interfering
with the process of central vestibular compensation (Box 5.2).
Examination of the Dizzy Patient
Clinical assessment includes auroscopy (Chapter 3), eye movements, and positional (Chapter 6)
and gait examination.
Table 5.4 Vertigo presentations: symptom triggers in patients with episodic vertigo
Trigger Possible cause
Lying down, turning over in bed Benign paroxysmal positional vertigo
Standing up Orthostatic hypotension
Neck movements Any vestibular disorder
Pressure changes/Valsalva Fistulas, superior canal dehiscence
Loud sounds Tullio’s phenomenon, superior canal dehiscence
Alcohol, exercise Episodic ataxias
Sleep deprivation, alcohol, foods, bright lights Vestibular migraine
BOX 5.2 FACTORS INTERFERING WITH CENTRAL VESTIBULAR COMPENSATION
• Fluctuating vestibular disorder (Meniere’s disease, vestibular migraine)
• Additional disorder:
Central nervous system
Peripheral nerve
Cervical spine
Visual
• Lack of mobility
• Drugs
• Visual dependence (‘visual vertigo’)
• Psychosocial issues
• Old age (+ many of the factors above)
28 e Ear
EVALUATION OF BALANCE
Eye Movements
e vestibular system provides a powerful input to the oculomotor system so eye movements
must be examined in detail (see Bronstein and Lempert 2017 for videos). e examination
has two broad aims:
1 To search for direct signs of a peripheral vestibular disorder, e.g. nystagmus, BPPV, or
a positive head thrust test.
2 To ensure non-vestibular mediated eye movements (saccades, pursuit) are normal,
excluding CNS lesions; patients must be clearly instructed to focus on a predetermined object with their eyes well illuminated.
e examination should assess six areas (see below). Diplopia or disconjugate appearance of
the eyes mandates formal cranial nerve III-IV-VI examination.
1 Spontaneous nystagmus is observed in primary (straight-ahead) eye position.
Document the waveform as sawtooth or jerky (and the fast-phase beat direction),
which is usually vestibular (peripheral or central), or pendular, quasi-sinusoidal nystagmus, without fast phases, which is central and non-vestibular.
Peripheral unilateral lesions induce vestibular tone bias between labyrinths and the eyes slowly
dri (just as the body) ipsilesionally. Quick-phase resetting the eyes straight ahead perpetuates
the nystagmus cycle, hence peripheral lesions are characterised by fast-phase ‘beating’ contral-
esionally. Vestibular nuclei lesions can follow this pattern, although, instead of being binocularly
conjugate and mostly horizontal, nystagmus oen shows major torsional (rotatory) components.
2 Gaze-evoked nystagmus is identied through patients xating on an object approxi-
mately 30° up-down and right-le; only very asymmetric nystagmus is pathological
in extreme gaze positions. Following an acute peripheral vestibular lesion, nystagmus
severity is classied as the following:
First-degree (on gaze deviation in direction of fast phase).
•
Second-degree (also present in primary gaze).
•
ird-degree (present even with gaze deviation to opposite direction to fast phase).
•
Nystagmus on gaze deviation can also indicate central lesions, frequently called
•
‘gaze-paretic’ because there is diculty holding an eccentric gaze. is can be
present in all gaze directions, as with cerebellar degenerations.
3 Smooth pursuit is examined with the patient tracking a slowly moving object that
they can see well. Abnormal pursuit means too many saccades to catch up with the
target, appearing jerky. Move the target slowly, otherwise everybody shows ‘broken
pursuit’. In principle normal pursuit rules out central vestibular disorders. Pursuit
performance decays signicantly with cerebellar-brainstem disease, age, alcohol and
CNS-acting drugs. Small horizontal plane asymmetries, if consistent, are signicant;
vertical plane asymmetries are common in normal subjects.
4 Saccades (fast eye movements) shi gaze between objects. Examine them with patients
keeping the head still and watching a pen or nger ick 20–30° up-down and rightle. e three independent properties to assess are velocity (normal/slow/absent, i.e.
gaze palsy), accuracy (normo-/hypo-/hypermetric), and binocular conjugacy (conjugate/disconjugate, as internuclear ophthalmoplegia). A small degree of hypometricity
can be normal; otherwise abnormalities are a strong sign of central disease.
e optokinetic nystagmus (OKN) system is not a truly separate oculomotor system. When
repetitive visual patterns, such as trac, move before our eyes, they follow an object with
smooth pursuit but intermittently the eyes are reset by fast, saccadic components. is
sequence of slow ipsidirectional following and fast contradirectional resetting movements
can be elicited with a rotating drum in front of the patient. Abnormalities of OKN follow
saccadic and pursuit movement rules, but slight oculomotor asymmetries are easier to see in
OKN. Peripheral vestibular lesions usually leave OKN unaected.
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EVALUATION OF BALANCE
Figure 5.1 The head-impulse test. The examiner holds the patient’s head with two hands and
delivers brisk head turns to one side and then the other, after resting for a couple of seconds. Top: a
normal response shows the eyes remain xed on the examiners nose. Bottom: abnormal response, or
positive HIT, is caused by lack of vestibular function. On the right labyrinth the eyes are carried with
the head and, in order to rexate on the examiner’s nose, a catch-up saccade has to be produced.
5 Vestibulo-ocular reex (VOR) acts to stabilise gaze during head movements through
slow-phase eye movements of equal velocity, but opposite direction, to head movement. VOR allows clear vision when walking, running, or head turning. Bouncing
images (oscillopsia) during such activities indicate bilateral vestibular function
loss. Manoeuvres assessing VOR in clinic use a fast version of the doll’s eyes-head
manoeuvre – the ‘head thrust’ or ‘head-impulse’ test (HIT) (Figure 5.1). Sit the patient
in front of you and ask him or her to xate a target on your face, e.g. nose. Hold
the patient’s head rmly and deliver fast, sudden head turns 10–15° on either side.
Catch-up saccades towards the target immediately aer head turns indicate failure of
the horizontal canal in the head turn’s direction.
e test identies acute and/or large unilateral peripheral vestibular decits, e.g. vestibular
neuritis. Chronic, compensated, incomplete unilateral lesions oen give negative or inconclusive results.
6 Positional manoeuvres are perhaps the single most important component of vestibu-
lar examination. BPPV is the most common and easily treated cause of vertigo, as
discussed in Chapter 6.
Clinical Examination of Postural Balance
Unsteadiness is associated with many disorders but if never associated with vertigo, dizziness, oscillopsia, or hearing disorder it is unlikely due to vestibular disease (see Bronstein
and Lempert 2017 for videos).
During Rombe rg’s tes t patients stand with feet as close together as possible and then
close their eyes. A Romberg-positive patient may actually fall, unlike normal subjects and
30 e Ear
EVALUATION OF BALANCE
patients with balance problems who only show some increase in body sway. It is positive in
patients with dorsal column disease, severe aerent polyneuropathy, and during the hyperacute phase of peripheral vestibulopathy, usually falling ipsilesionally. e most dramatic
Romberg’s tests are seen in functional (psychogenic) disease. Always show patients that you
are ready to catch them should they fall.
Postural reexes become important in examination of patient’s dizziness, which cannot
be explained by the vestibular system. ey are elicited by pushing and pulling the upper
trunk, whilst standing behind the patient (avoiding anticipation). Postural responses may
be absent in parkinsonian patients who can fall log-like unless caught; a few shuing steps
prevent this in early stages. In cerebellar syndromes, trunk pulls may unmask trunk titubation. Elderly patients with fear of falling exhibit a startle response. Vestibular patients may
be unsteady, but the response pattern is preserved.
During gait examination, neurological balance disorders show problems with step initiation
(frontal lesions, parkinsonism), steady-state stepping (parkinsonism, spasticity), broad-base
gait (cerebellar, bilateral vestibular failure), or arm movements (parkinsonism). Patients with
fear of falling reach out arms as if expecting to fall and step with apparent unnecessary care;
this may be a psychogenic reaction oen triggered by a vestibular, vascular, or fall episode. If
gait is normal, examine tandem walking (heel to toe) or with eyes closed. In unilateral vestibular lesions, particularly the acute stage, patients may deviate ipsilesionally. In Unterberger’s
test, on-the-spot eyes-closed walking reveals an ipsilesional deviation.
Laboratory Assessment of Vestibular and Oculomotor Function
Most balance disorder patients do not require eye movement recordings (oculography or
nystagmography). Recordings may be useful to
1 Establish if spontaneous nystagmus is acquired or congenital,
2 Ascertain a potentially signicant abnormality, e.g. internuclear ophthalmoplegia if
clinical examination of eye movements cannot, and
3 Measure vestibular function.
Vestibular conditions diagnosed clinically or with other investigations (audiograms, magnetic resonance imaging [MRI] scans) do not necessitate oculography, e.g. BPPV, vestibular
neuritis, vestibular migraine, Meniere’s disease, and vestibular schwannomas.
Caloric tests activate the horizontal semicircular canal via temperature changes in the
external auditory canal. Irrigation can be water or air, usually at 30°C and 44°C. Air
irrigation allows testing with eardrum perforations, but responses are less consistent. e
supine subject has the head raised 30° so the horizontal canal assumes an approximately
vertical position. Cold irrigation induces horizontal nystagmus beating the opposite
direction, and ipsilaterally during warm irrigation (cold-opposite-warm-same; COWS).
Computerised measurements are taken of the slow-phase velocity of the nystagmus but
naked-eye measurement of nystagmus duration is reliable. ere are four main abnormalities of caloric responses:
1 Bilateral absence: Ototoxicity, post-meningitis, idiopathic, artefact due to poor tech-
nique or wax.
2 Unilateral canal paresis: One ear shows reduced/absent response (vestibular schwan-
noma or vestibular neuritis).
3 Directional preponderance (DP) of nystagmus: is is essentially a right-le asym-
metry in VOR. An acute le vestibular neuritis initially shows le canal paresis and
spontaneous right-beating nystagmus but, aer recovery, may only show right DP. DP
is a non-specic nding with poor localisation value.
4 Abnormal VOR suppression: Vestibular nystagmus is suppressed by visual xation,
so lack of suppression is a good central sign. To do this the caloric response has to be
measured comparatively in the dark and under visual xation.
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EVALUATION OF BALANCE
Computer-controlled chairs for rotational testing are available in few specialised departments. However, patients can be rotated on any swivel chair for 30 seconds, timing the nystagmus on stopping rotation. Rotational tests are a good way of measuring the overall level of
vestibular function, e.g. remaining vestibular function following ototoxicity.
Video head-impulse test (vHIT) systems are now commercially available. Detecting corrective ‘catch-up’ saccades aer an operator-delivered head thrust becomes easier, thus
indicating vestibular insuciency. e gain of the VOR (peak eye velocity/peak head
velocity) is also measured. Discrepancies between clinical HIT, vHIT, and caloric tests is
not always due to technical problems; vHIT tests high-frequency VOR whereas the caloric
test examines the low-frequency response. us, a patient with Meniere’s disease may have
abnormal caloric results but normal vHIT. ree-dimensional (3D) vHIT systems assess
all six semicircular canals, but this adds little to the day-to-day management of most vestibular patients.
Posturography and Vemps
Posturography records postural sway usually with force platforms. Recordings with eyes
open and closed quantify the Romberg’s test. Dynamic posturography adds balance stimuli
(moving platform, visual stimuli). Posturography advances understanding of postural systems but oers limited day-to-day clinical value.
Cervical vestibular myogenic evoked potential (cVEMP) is the only routine test of vestibulo-spinal function. VEMPs are electromyographic potentials elicited in sternomastoid
muscles by loud clicks delivered to each ear individually. Conductive deafness prevents
clicks reaching the labyrinth, abolishing the response, so otoscopy and audiometry are
necessary. VEMPs identify Tullio’s phenomenon and third window disorders, such as
superior canal dehiscence, where the symptomatic ear generates low-threshold, highamplitude potentials. It is argued that the main structure activated by sound is the saccule,
so cVEMPs are considered an otolith test. Ocular VEMPs may be mediated via the utricle
more than the saccule. Ideally, absent VEMPs would imply a selective otolithic disorder
but, unfortunately, the meaning of an isolated VEMP abnormality is unclear, particularly
in older patients.
Acknowledgements
e author is grateful to Drs. Alex Charlton and Simon Cole for their useful feedback and
suggestions.
KEY POINTS
• Dizziness may indicate vestibular disease but equally general medical, cardiovascular,
or neurological disorders can be the cause.
• Rotational vertigo usually indicates vestibular system disease, but the lesion may be
anywhere from the semicircular canals up to the cerebral hemispheres.
• History taking is the key to diagnosis, but examination of the eye movements, the
positional manoeuvre, and hearing levels are a close second.
• Audio-vestibular tests are not essential for diagnosis in most cases.
• A summary of examination ndings and tests is as follows:
• Positional manoeuvres are perhaps the single most important component of
vestibular examination.
• During spontaneous nystagmus, in peripheral unilateral vestibular lesions, the
eyes slowly drift (just as the body) ipsilesionally, with eye resetting by fast-phase
‘beating’ contralesionally.
• Smooth pursuit, saccades, and OKN become impaired with central (cerebellar-
brainstem) disease. Peripheral vestibular lesions usually leave these unaffected.
• VOR (measured by ‘head thrust’ or HIT) is impaired in acute and/or large unilateral
peripheral vestibular decits, e.g. vestibular neuritis.
32 e Ear
VESTIBULAR DISORDERS AND REHABILITATION
• cVEMPS are the only routine test of vestibulo-spinal function to identify third window
disorders such as superior canal dehiscence with low-threshold, high-amplitude
potentials. They are absent in conductive hearing loss.
• Romberg’s test is positive if a patient falls ipsilesionally in hyper-acute peripheral
vestibulopathy, dorsal column spinal disease, and afferent polyneuropathy.
• Caloric tests activate the lateral semicircular canal via temperature changes (30°C and
44°C). Cold irrigation induces horizontal nystagmus beating the opposite direction,
and ipsilaterally during warm irrigation.
• vHIT detects vestibular insufciency through corrective catch-up saccades. It tests
high-frequency VOR, whereas the caloric test examines the low-frequency response.
Meniere’s disease demonstrates abnormal caloric results but normal vHIT.
Further Reading
1. Bronstein A and Lempert T. Dizziness, a Practical Approach to Diagnosis and
Management. 2nd ed., Cambridge, UK: Cambridge University Press, 2017.
2. Lee SH, Kim JS. Dierential diagnosis of acute vascular vertigo. Curr Opin Neurol.
2020, 33(1):142–149. doi: 10.1097/WCO.0000000000000776.
3. Seemungal BM, Bronstein AM. A practical approach to acute vertigo. Pract Neurol.
2008, 8(4):211–21. doi: 10.1136/jnnp.2008.154799. Review. Erratum in: Pract Neurol.
2009, 9(1). doi: 10.1136/jnnp.2008.154799corr1.
6. VESTIBULAR DISORDERS AND REHABILITATION
Acute Unilateral Peripheral Vestibulopathy (AUPVP)
Acute unilateral peripheral vestibulopathy (AUPVP) is a clinical syndrome caused by acute
vertigo (onset over hours or days) with nausea and vomiting, oscillopsia, ipsilateral lateropulsion, and gait instability, occurring as a result of vestibular tone imbalance.
On exam ination the uni lateral loss of vest ibular func tion is associated w ith a positive head th rust
test ipsilaterally, and horizontal-torsional nystagmus beating ipsilaterally. Hearing is preserved.
Pathophysiology
e pathophysiolog y of AUPVP is not f ully understood. ere is some circu mstantial e vidence
for a viral aetiology, from autopsy studies, from animal models, and from genome-wide association studies. ere is also evidence of vascular aetiology in some cases, including evidence
of pro-inammatory state and associations with specic HLA subtypes. e term AUPVP
incorporates both neural and end-organ pathologies, rather than using terms which presuppose a specic site of lesion or pathophysiology (vestibular neuritis, vestibular neuronitis).
Clinical assessment of the nystagmus and head impulse abnormality, supplemented by vestibular diagnostic tests (video head-impulse test, caloric, ocular, and cervical video evoked
myogenic potential) can allow the dierentiation into isolated superior or inferior vestibular
nerve pathology, or complete varieties (see Chapter 5). ese subtypes have diering presentations, prognoses, and rates of complications such as benign paroxysmal positional vertigo
(BPPV). Imaging is usually normal, although in exceptional cases neuritis can be seen on
magnetic resonance imaging (MRI).
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VESTIBULAR DISORDERS AND REHABILITATION
Management
Management is largely supportive, with medical management of nausea and vomiting. Expert
consensus is to recommend early mobilisation and/or vestibular rehabilitation (VR) as tolerated, and to minimise use of vestibular sedatives, since this is believed to slow recovery. e
use of corticosteroids is controversial and further evidence is awaited from ongoing trials.
Prognosis
e prognosis is variable with persistent symptoms in a signicant proportion. Predictors of
poor recovery include visua l dependency, high levels of an xiety, and maladaptive illness beliefs.
e relapse rates for AUPVP seem to be very low (around 2% in 5 years), meaning recurrent
episodes should arouse suspicion of another disorder such as vestibular migraine (VM).
Meniere’s Disease (MD)
Meniere’s disease (MD) is an idiopathic inner ear disorder characterised by recurrent spontaneous vertigo episodes characteristically at least 30 minutes long. It is accompanied by
uctuating or progressive sensorineural hearing loss (SNHL), tinnitus, and aural fullness in
the aected ear.
MD is highly linked to endolymphatic hydrops (ELH), although ELH is not pathognomonic
of MD. Autoimmune, viral, allergic, and vascular hypotheses have all been proposed as
underlying causes and all have some circumstantial support, but a single unifying aetiology remains elusive. e condition is most common during the working adult age range. A
minority of cases (<15%) appear to be familial and there are a number of candidate genes,
some of which link to ion transport.
Diagnosis
Diagnosis is based on a set of criteria derived from expert opinion. Diagnostic criteria for
‘denite’ and ‘probable’ cases are shown in Table 6.1.
1
ere is associated nystagmus when the patient is seen around the time of an attack. In the
irritative phase, the fast phase of nystagmus will beat towards the aected ear in a horizontal
or horizontal-torsional direction, a nding which usually lasts less than 1 hour. In the paretic
Table 6.1 Diagnostic criteria for Meniere’s disease and vestibular migraine from The International
Headache Society (IHS) 2018
Diagnosis Criteria
Denite Meniere’s
disease
Probable Meniere’s
disease
Vestibular migraine 1 At least ve episodes with vestibular symptoms of moderate or severe
34 e Ear
2
1 ≥2 denitive spontaneous episodes of vertigo lasting 20 minutes to
12 hours +
2 Audiometrically documented low-to medium-frequency sensorineural
hearing loss in the affected ear on at least one occasion before,
during, or after one of the episodes of vertigo +
3 Fluctuating aural symptoms (hearing, tinnitus or fullness) in the
affected ear
1 ≥2 episodes of vertigo or dizziness, each lasting 20 minutes to
24 hours +
2 Fluctuating aural symptoms (hearing, tinnitus or fullness) in the
affected ear
intensity lasting 5 minutes to 72 hours
2 History of migraine according to IHS classication
3 Migraine feature with >50% of attacks:
• Headache with two of: unilateral, throbbing, moderate–severe
• Aggravation by movement
• Photo- and phonophobia
• Visual aura
4 Not better accounted for by another disorder
VESTIBULAR DISORDERS AND REHABILITATION
phase, the fast phase of nystagmus will beat away from the aected ear and last hours to days.
In the recovery phase the nystagmus again beats towards the aected side because peripheral
vestibular function recovers.
SNHL characteristically aects the low frequencies. Occasionally patients experience drop
attacks (also called Turmarkin or otolithic crisis) where there is a sudden drop to the ground
without loss of consciousness, or associated vertigo. Bilateral MD does occur, but in the
majority of cases the condition is unilateral, at least initially. Estimates of rate of bilateral
disease are highly variable; one estimate is 47% within 20 years of onset.
Other investigations can include an MRI of the brain and internal auditory meatus (mainly
to rule out retrocochlear causes) and electrocochleography (an increased summation
potential:action potential ratio (>0.45) is supportive of the diagnosis). Use of gadolinium-
enhanced MRI to image ELH directly is a promising and evolving technique.
Management
Dietary restrictions on sodium and caeine are traditionally advised, although not proven.
ere is mixed evidence for the use of betahistine in MD, although it does have a favourable
safety prole and is well tolerated, so it is oen used. A Cochrane review concluded that there
is no evidence to demonstrate the eectiveness of positive transtympanic low-pressure therapy. Diuretics have also been recommended, although the evidence base is weak and there is
potential for signicant unwanted eects in relation to salt homeostasis and renal function.
ere is some evidence to support the eectiveness of intratympanic steroids. Endolymphatic
duct surgery and vestibular nerve section are surgical options for refractory cases that allow
hearing preservation. Intratympanic gentamicin and labyrinthectomy tend to be reserved
for patients with signicant SNHL or refractory symptoms due to the risks of worsening
hearing (3–21% rate of hearing loss for low-dose gentamicin injections, complete hearing loss
for labyrinthectomy) or causing persistent vestibular dysfunction.
Supportive treatments for hearing loss, tinnitus, and persistent interictal vestibular symptoms (VR) should be oered where applicable.
Benign Paroxysmal Positional Vertigo (BPPV)
BPPV is a common cause of episodic vertigo with a lifetime prevalence of 2.5%. It is a disorder of the otoconia, which are calcium carbonate crystals normally embedded in the macula
of the utricle and saccule.
ere are two theories about how BPPV occurs: canalolithiasis and cupulolithiasis.
Canalolithiasis is thought to be more common, and it occurs when the detached otoconia are
free oating, but these cause cupula deformation by exerting a plunger eect on the endolymph when stimulated to move by gravity. In cupulolithiasis, degenerative otoconia adhere
to the cupula making it more gravity sensitive.
All three horizontal canals can be aected in BPPV, but the majority of cases (over 93%)
occur in the posterior canal (PC-BPPV), with the horizontal canal aected in around 5%.
Anterior canal BPPV is very rare. is distribution is explained by the natural anatomical
orientation of the canals.
e hallmark of PC-BPPV is vertigo lasting seconds on lying down, sitting up from the lying
position, or rolling in bed and when extending or exing the neck.
ese symptoms can present in clusters with several attacks per day. In between attacks or
shortly aer successful treatment, patients are either symptom free or experience a sensation
of imbalance. However, some patients may report atypical symptoms, and it is worthwhile
conducting the positional tests in all patients presenting with episodic vertigo, older adults
with falls or imbalance, or aer a head injury.
BPPV can occur in isolation or in association with other conditions like AUPVP, MD, or
head injury.
e Ear 35
VESTIBULAR DISORDERS AND REHABILITATION
Diagnosis
Diagnosis is made on the basis of typical signs (nystagmus) and symptoms (vertigo) provoked by specic positional tests in each plane for each pair of canals: le anterior and right
posterior (LARP), right anterior and le posterior (RALP), and the horizontal canals.
e posterior and anterior canal pairs are stimulated when performing the Dix-Hallpike
test (Figure 6.1). e patient is seated along the couch, feet up, and the head is turned 45°
towards the side being tested, aligning the vertical canals with the sagittal plane. e head is
Figure 6.1 Epley’s repositioning manoeuvre. Left posterior canal BPPV. The patient is sat on the
table with the head turned 45° to the left side (affected side) (a), and (b) brought down rapidly
with the head still turned 45° to the affected side and extended over the edge of the table, 30°
below the horizontal plane. Note that the neck is well supported (inquire about neck pathology
before the test). (c) The head is then turned 90° to the opposite side (right). (d) This is followed by
rotating the head and body 90° facing downwards (135° from the supine position). (e) The legs
are then displaced over the side of the table in anticipation of a return to a seated position, and
(f) the patient is brought to a sitting position with the head turned forward.
36 e Ear
VESTIBULAR DISORDERS AND REHABILITATION
brought down briskly over the end of the couch to lie 30° below the horizontal while maintaining a position 45° to the side being tested. Patients should be counselled prior to the test
to expect vertigo, but they still need to try and maintain their eyes open for examination.
In PC-BPPV, the fast phase of the resultant nystagmus is upwards and outwards (upbeating
geotropic-torsional nystagmus), whereas in anterior canal BPPV the nystagmus is downward
and inwards. e LARP canals are stimulated during the right Dix-Hallpike test and the
RALP canals in the le Dix-Hallpike test.
Lateral canal BPPV is assessed using the roll test. e head is exed 30°, bringing the horizontal canal into the vertical plane, and it is then briskly rolled to one side. e same is
repeated on the opposite side. In the majority of cases the nystagmus will be horizontal and
geotropic and towards the ear being tested, and it will be present on rolling both sides, even
with a unilateral lesion.
It is important to discriminate BPPV from positional vertigo arising from central pathology.
Neurological disorders that can cause positional vertigo include VM, vertebrobasilar insufciency, demyelinating lesions, and central nervous system (CNS) lesions. Drugs can also
cause positional vertigo.
An MRI of the brain including the posterior fossa a nd internal auditory meatus is required when
Nystagmus is atypical for any of the BPPV syndromes.
•
Brainstem or cerebellar signs are present.
•
Positional vertigo does not resolve with repeated therapeutic manoeuvres.
•
Management
e canalith repositioning procedure (CRP) is based on the theory of ‘canalolithiasis’ and
seeks to move the particles from the PC into the utricle via the common crus. A recent
Cochrane meta-analysis has found that the CRP on its own is eective in almost 80%
of cases. e Epley manoeuvre is described in Figure 6.1. ere are alternative eective
manoeuvres for PC-BPPV (e.g. modied Semont) and for lateral canal BPPV (log roll or
barbecue manoeuvre). Brandt Daro exercises are well known but are less eective than
repositioning manoeuvres, so they should not be considered as a rst-line treatment.
Recurrence of BPPV is common, so patients should be educated on what to do in this
eventuality. Surgery (semicircular canal occlusion) is considered in a very small number
of refractory cases. Although eective, this procedure has risks of SNHL and chronic
imbalance.
Vestibular Migraine (VM)
Migraine is common and almost everyone will either have experienced the condition personally or have friends, family, or other acquaintances who are suerers. Migraine is a neurovascular condition in which the headache is thought to originate via activation of the
trigeminovascular reex; the trigeminal nerve innervates the meninges mediating the pain
that is migraine’s most notorious clinical feature. VM is a subtype of migraine in which vestibular symptoms predominate.
Diagnosis
Diagnosis is made according to clinical criteria (Table 6.1) based around the presence of epi-
sodic vertigo with associated migrainous features including headache and sensory sensitivity (photophobia, phonophobia) and aura.
e physical examination of patients with VM in the interictal period is usually normal.
However, some patients report signicant visual motion intolerance that can be detected
during eye movement examination. One study of patients with VM in the acute setting
found a range of eye movement abnormalitie s including positiona l nystagmus, sponta neous
2
e Ear 37
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