Introduction

- this guidemap is mainly focused on the clinical features that help differentiate acute
peripheral vertigo (due to unilateral peripheral vestibular disease) from acute central
vertigo (due to cerebellar or brainstem disease)

- this guidemap will also offer some guidance on how to approach the problem of
recurrent episodic vertigo and acute positional vertigo

- the most important initial determination that needs to be made in a patient with acute
dizziness is to determine whether the patient's dizziness represents true vertigo - rather
than being due to some other specific/non-specific syndrome causing dizziness eg. non-
specific lightheadeness or near-syncope/pre-syncope or dysequilibrium syndrome

- the patient should be asked to "describe his dizziness" without the use of leading
questions

Vertigo = sensation of disorientation in space with a sensation of motion where no

motion exists, and the sensation may be swaying, tilting or rotational in character

- mild vertigo may produce a feeling that the earth is moving or tilting slightly, or it may
produce a vague sensation of motion-sickness, or a feeling that one is being pulled to the
side; while severe vertigo may produce a distinct whirling sensation with prominent
autonomic symptoms of nausea and vomiting and sweating and pallor

- vertigo is due to a mismatch of two-or-more of the vestibular, visual and proprioceptive

inputs to the vestibular system and thus any unilateral lesion of the vestibular
apparatus/pathways may produce vertigo

Oscillopsia = the visual (to-and-fro) illusion of enviromental movement, not

accompanied by vertigo or a sensation of motion, and it signifies a bilateral decrease in
vestibular function eg. secondary to ototoxic drugs (aminoglycosides, loop diuretics) or
due to bilateral structural vestibular nerve damage eg. bilateral acoustic neuromas

- the patient with oscillopsia (due to bilateral vestibulopathy) does not complain of
vertigo, although he may have a sensation of blurred vision or decreased visual acuity or
spatial disorientation during head motion, especially when turning the head rapidly from
side-to-side or when ambulating in a dark enviroment or spatial enviroment with too
many blurring visual distractions eg. busy city street

- the patient with oscillopsia (due to bilateral vestibulopathy) may have difficulty reading
street signs unless the head is held perfectly still, and he may have to stop walking to
keep his head sufficiently still
- the patient with oscillopsia (due to bilateral vestibulopathy) may have poor balance
when walking in the dark (when visual cues are absent) or on uneven surfaces such as
gravel (which causes the head to lurch about)

Near syncope/pre-syncope = the sensation is that of "graying-out", lightheadedness,

generalized weakness, or a sudden overwhelming feeling that one is going to "pass-out"

- the feeling can occur suddenly without warning in any postural position, or be
precipitated by suddenly standing, or occur during heavy exertion

- cardiovascular pathology or volume depletion is responsible for the majority of cases

Dysequilibrium = a feeling of unsteadiness or imbalance, without an actual illusion of

movement and without a sensation of faintness and usually more noticeable when the
patient walks or stands unassisted eg. secondary to 'multi-sensory' deficits in elderly
patients

(* Dysequilibrium and poor gait - without true vertigo - can also be caused by occult
hydrocephalus, a chronic subdural hemorrhage, Parkinsons's disease or multi-infarct
syndome)

Non-vestibular dizziness = a vague sensation of wooziness or wobbliness, floating

sensations, feeling "spaced-out", feeling depersonalized or detached from one's body,
feeling that "one is spinning inside one's head"

- the feelings may be precipitated by stressful conditions eg. driving on a busy highway
or during a domestic argument

- many of these patients have "psychogenic dizziness"

- if the patient definitely has acute vertiginous symptoms, then the next most important
determination that needs to be made in a patient with definite acute vertigo is to
determine whether the acute vertigo fits into a particular clinical pattern, and whether the
vertigo is:-

 an acute vertigo of sudden onset

 a recurrent episode of episodic vertigo
 an acute positional vertigo

- each of these presentations has a different set of possible differential diagnoses and each
presentation requires a different clinical approach
History of the present illness

- first confirm that the dizziness is vertiginous in nature, and not suggestive of near-
syncope or non-vestibular dizziness
- secondly, confirm that the dizziness is affected by movements of the head, which
suggests a peripheral vertigo

 a patient with peripheral acute vertigo often prefers to sit upright and not lie
down, or prefers to lie still with the unaffected ear undermost; and the patient also
prefers to avoid any sudden head movements
 a patient with central vertigo usually has a lesser degree of dizziness, which is far
less affected by head movements and not specifically related to a particular head
position

(* a sensation of acute vertigo can be precipitated in normal people - even with the head
kept perfectly still - if there is sudden, extreme and continuous movement of visual
targets; and this phenomenon of visual vertigo is different from acute peripheral vertigo,
which is worsened by movements of the head and not by movements of the eyes or visual
targets)

- determine whether the vertigo is positional in nature

 a history of episodic vertigo lasting seconds, which is only precipitated by

sudden movements of the head (looking up, suddenly twisting the head,
suddenly getting up from a supine position or when suddenly rolling over in bed)
suggests benign positional vertigo (especially if the patient is middle-aged or
elderly; BPV is commoner in females)
 a patient with benign positional vertigo may be able to identify a particular
movement or position of the head that precipitates vertigo, which usually occurs
after a latent period of 10 - 20 seconds
 patients with BPV may complain of non-specific nausea, dysequilibrium and
dizziness between attacks

(* benign paroxysmal vertigo of childhood may occur in young children (1 - 5 years of

age) and be difficult to diagnose, and may present as paroxysmal torticollis - carefully
inquire of the parents whether there are any abnormal eye movements during these
paroxysmal episodes; patients with postural pre-syncope may develop dizziness with
standing, but not with head turning when supine)

- establish whether associated autonomic symptoms are present

 a patient with severe acute peripheral vertigo may have prominent autonomic
symptoms (nausea, vomiting, sweating, pallor)
 prominent autonomic symptoms are far less common in patients with central
vertigo

- determine the speed of onset and the duration of the vertigo

- sudden onset vertigo can be due to peripheral or central vertigo, and it may not be
possible to differentiate between the two clinical syndromes if there are no associated
otological or neurological symptoms to offer additional clinical clues

- the duration of the vertigo provides useful information

 vertigo lasting seconds => suggests benign paroxysmal positional vertigo

 vertigo lasting minutes => suggests transient cerebrovascular ischemia (posterior
circulation TIA)
 vertigo lasting hours => suggests Meniere's syndrome
 vertigo lasting hours-days => suggests vestibular neuronitis or posterior
circulation strokes

- a patient with acute peripheral vertigo secondary to vestibular neuronitis (the cause
in 90% of cases in young patients with acute-subacute vertigo) often has dizziness that
starts suddenly or gradually, and worsens over a few hours before spontaneously
adapting/waning over a time period of 24 - 48 hours => the vertigo usually resolves
completely over several weeks, although a variable sense of imbalance may persist for
months

- a patient with acute central vertigo due to a posterior circulation stroke may have a
lesser degree of dizziness that often has a more persistent course, and the vertigo does not
necessarily adapt/wane within the next 12 - 48 hours; the patient often has accompanying
posterior circulation neurological symptoms

- an acute episode of vertigo lasting only a few minutes suggests a vertebro-basilar

artery TIA - especially if occurring in a patient with known cardiovascular risk factors
(elderly, known vascular disease, CAD, AF, hypertension, smoker, diabetes mellitus) and
especially when associated with posterior circulation neurological symptoms

- an isolated episode of sudden-onset vertigo that only lasts a few hours may be due to
the first episode of Meniere's disease, which very rarely presents initially without the
usual associated otological symptoms

- determine whether there are any associated otological or neurological symptoms

- associated otological symptoms (deafness and/or tinnitus) suggests peripheral

vertigo

 many patients with vestibular neuronitis have a history of a recent viral illness in
the past few weeks, and the presence of otological symptoms in a patient with
acute vestibular neuronitis suggests acute (serous) labyrinthitis
 recent severe earache +/- ear discharge +/- fever suggests a middle ear infection
and a possible acute (purulent) labyrinthitis
  recent head trauma, sudden coughing/sneezing + sudden 'pop' in the ear, or recent
scuba diving suggests a possible peri-lymphatic fistula (vertiginous symptoms
may also be exacerbated by valsalva-type maneuvers or a loud noise)
 recent significant head trauma suggests labyrinthine concussion, or possible
ossicular disruption, or a temporal bone fracture with damage to the cochlea
or internal auditory nerve

(* a patient with central vertigo due to a TIA or stroke only affecting the internal auditory
artery - labyrinthine apoplexy - may present with vertigo + sensorineural hearing loss +
no associated neurological symptoms, and can be nearly impossible to clinically
differentiate from acute labyrinthitis)

- associated posterior circulation neurological symptoms suggest central vertigo

- posterior circulation stroke syndromes may present acutely and the stroke may be
complete/incomplete, and the patient may have any of the following symptoms/signs:-

 numbness of the arms or legs

 weakness of the arms or legs
 clumsiness of the arms or legs with overshoot/undershoot phenomena
 face pain or hypoesthesia
 double vision, blurred vision
 decreased vision or tunnel vision
 patient and/or outside observer notes dysconjugate eye movements, gaze palsies
and/or central nystagmus
 patient and/or outside observer notes incomplete eye adduction (internuclear
ophthalmoplegia)
 patient and/or outside observer notes vertical eye deviation (skew deviations)
 patient and/or outside observer notes ptosis and/or small pupil (Horners
syndrome)
 difficulty with swallowing (dysphagia)
 difficulty with speaking (dysarthria)
 hoarse voice (dysphonia)
 face weakness (7th cranial nerve)
 palatal speech (9th and 10 th cranial nerve)
 "dissociated" sensory loss of one half of the body (loss of pain/temperature
sensation greater than loss of proprioception)
 "crossed" sensory loss (loss of pain/temperature sensation of the ipsilateral face
and contralateral trunk and limbs)
 ataxic gait

(* the absence of associated neurological symptoms does not exclude central vertigo
because as many as ~ 25% of middle-aged/elderly patients with risk factors for stroke,
who present to the ED with isolated severe vertigo + postural instability may have an
inferior cerebellar infarction)
- after determining the speed of onset and duration of the vertigo + presence of any
otological or neurological symptoms => determine whether the patient has a history of
previous episodes of vertigo

- a history of previous episodes of temporary dizziness lasting a few hours suggests

Meniere's disease - especially if there is a history of associated ear fullness/pressure,
poor speech discrimination in loud enviroments, fluctuating but progressive hearing loss
(especially to low frequencies) and associated tinnitus; the recurrent attacks of vertigo
may occur in clusters with long symptom-free intervals

- a history of previous episodes of temporary vertigo lasting minutes suggests

vertebro-basilar artery TIAs, which may precede a full-blown stroke by days-to-weeks

- a patient with temporal lobe seizures will likely have associated symptoms -
hallucinations, memory impairment, automatic behaviour, trance-like states and motor
seizures (nystagmus is only seen when the seizure arises in the labyrinth =
vestibulogenic seizure)

- a patient with basilar migraine is usually a young female and the patient will often
develop a typical migraine headache concurrently with the vertigo, or after the onset of
the vertigo, and the patient will usually have a previous history of recurrent attacks or a
strong family history of basilar migraine (associated neurological symptoms - dysarthria,
ataxia, blindness, deafness, tinnitus, confusion, sensorial clouding - are usually also
present) => the diagnosis of basilar migraine can be missed if a typical migraine
headache does not occur and the patient is then often incorrectly presumed to have a
psychiatric condition

Examination

- vital signs and a detailed cardiovascular exam is required to exclude cardiac or

vascular causes of near-syncope if the dizziness is not definitely vertiginous in character

- atrial fibrillation and secondary embolisation may be the cause of a cerebellar or brain
stem stroke

- auscultate the neck for bruits (vertebral artery insufficiency secondary to a subclavian
steal syndrome, vertebral artery dissection or vertebral artery stenosis)

- auscultate the head for bruits in patients with pulsatile tinnitus (glomus tumor,
aneurysm/dissection of the internal carotid artery)

- examine the ear for signs of cerumen impaction, an earcanal FB, evidence of otitis
media or a choleastoma or a perforated eardrum or a hemotympanum (secondary to
trauma) - they can all be associated with acute vertigo
- determine whether there is any hearing loss by determining how far from the ear a
finger-rub can still be heard (compare sides)

- any hearing loss should be further differentiated as either a conductive or

sensorineural hearing loss by doing the Rinne test (put a 256Hz tuning fork on the
mastoid and determine for how many seconds the sound can be heard => repeat the test
with the tuning fork held in the air about 1 inch from the external auditory meatus = > if
bone conduction is better than air conduction = conductive hearing loss)

- the Weber test (performed by placing a tuning fork in the center of the forehead)
confirms an unilateral conductive hearing loss by localising the sound to the affected
side, but is referrred to the unaffected side when there is an unilateral sensorineural
hearing loss

- perform the fistula test if you suspect a peri-lymphatic fistula (a simplified fistula test
can be performed by pressing the tragus rapidly towards the earcanal so as to quickly
occlude the earcanal opening => induced vertigo +/- nystagmus is a positive test =
Hennebert's sign)

- perform a complete neurological examination including all the following

observations:-

 mental status
 cranial nerves
 sensorimotor exam of the limbs
 speech evaluation for dysarthria and/or dysphonia
 swallowing assessment for dysphagia
 finger-nose and heel-knee testing for dysmetria
 rapid hand movement testing for dysdiadochokinesis (fine motor coordination)
 gaze preferences at rest
 whether the eyes move conjugatedly in all directions of gaze without
overshoot/undershoot phenomena and secondary corrective step-oscillations
(saccadic testing)
 smoothness of visual pursuit eye movements (using your moving finger as a
visual target in all directions of gaze)
 visual acuity and confrontational visual fields
 presence of a Horner's syndrome

- checking for gait ataxia (= getting the patient to stand and then evaluating the patient's
ability to walk) is a critical part of the neurological examination
 a patient with acute vestibular ataxia is very disinclined to walk, but the patient
can usually walk if strongly ecouraged/coaxed to walk
 a patient with acute vestibular ataxia has a tendency to list or fall or veer or
stagger towards the affected side
 a patient with acute vestibular ataxia has a greater inability to maintain his
balance when standing or walking with the eyes closed, because of the loss of
 visual cues that can counterbalance the vestibular impairment (* perform an
enhanced Romberg test by asking the patient to stand upright with the eyes
closed => then ask the patient to march on the spot => the patient will tend to
rotate towards the side of the lesion - called a positive Fukuda or Unterberger test)
 a patient with acute cerebellar ataxia due to a cerebellar/brain stem stroke may
have extreme truncal ataxia and a total inability to stand or even take a single step
without falling, and there is no definite tendency to tilt or fall to any particular
side => an ED physician may mistakenly conclude that the patient will not walk,
when he cannot walk
 however, a patient with acute cerebellar ataxia may occasionally only have mild
truncal ataxia that is unaffected by closing the eyes, and subtle truncal ataxia
(slight unsteadiness when turning around or changing direction) may be difficult
to differentiate from the poor balance found in patients with severe peripheral
vertigo

(* see the gait disorder, frequent falls, and drop attacks guidemap for further problem-
solving information that can help differentiate the various causes of ataxia)

- carefully check for nystagmus

 the direction of nystagmus is defined by the direction of the fast phase

 peripheral nystagmus is often decreased in speed or intensity or even totally
eliminated by visual fixation => so test for nystagmus by avoiding visual fixation
(the patient should stare vaguely into the distance and should then be instructed to
first look 45 degrees to the left and then 45 degrees to the right, and not be
instructed to follow the examiner's finger as per the usual testing technique)
 nystagmus seen only when fixation is inhibited implies a peripheral nystagmus
 peripheral nystagmus is usually horizontal (or horizonto-rotatory) and jerking in
nature with the fast phase away from the affected ear, and the intensity of the
nystagmus increases (or the nystagmus is only present) when looking towards the
fast phase of the nystagmus and away from the affected side (Alexander's law)
 peripheral nystagmus always beats in the same direction, even when the direction
of gaze changes from left-to-right or vica versa
 peripheral nystagmus may have a rotatory torsional component, but is never
vertical or purely torsional
 peripheral spontaneous nystagmus is usually only prominent during the first 12 -
24 hours and may be inhibited completely within a few days - even in the
direction of the fast phase
 peripheral nystagmus is often absent if the patient is examined when
asymptomatic
 central nystagmus may be spontaneously present at rest when the patient is
staring straight ahead, it is often unaffected by visual fixation, it may occur in one
or multiple directions of gaze, it may change beat-direction in different directions
of gaze, it may be purely vertical or purely torsional or purely horizontal, and it
may persist for weeks-months
- if nystagmus is not present at rest or provoked by eccentric gaze => further
provocative maneuvers should be utilized to try and induce vertigo and nystagmus
(because the vertigo and nystagmus associated with benign positional vertigo may only
be provoked in certain head positions)

- a common provocative test is the Dix-Hallpike maneuver

 sit the patient upright on a stretcher with his head extending just above the top of
the bed and with his head rotated 45 degrees to the left => instruct the patient to
keep his eyes open, but to avoid visual fixation by staring into the distance =>
warn the patient that you are going to suddenly drop the back of the bed, which
may induce increased vertigo, but that the patient must avoid closing his eyes
during the test => slowly drop the back of the bed to a horizontal (or 30 degrees
below horizontal tilt) and ensure that the patient's head is extended about 45
degrees back off the end of the bed => observe for nystagmus for about 30
seconds => repeat the test with the head rotated 45 degrees to the right to compare
sides
 a patient with peripheral vertigo may develop nystagmus after a latent period of
10 - 15 seconds, the nystagmus will be of the typical horizonto-torsional jerking
type, the nystagmus will fatigue and disappear after about 20 - 30 seconds, and
the nystagmus will not appear on repeat testing because it shows adaptability (the
affected side is the side with the ear undermost)
 a patient with central vertigo may develop nystagmus (often purely vertical) that
appears immediately, persists and does not fatigue over time, and which does not
adapt by disappearing on repeat testing
 a patient with benign positional vertigo will develop nystagmus, that has a 3 - 10
second latent onset, that intensifies and then gradually resolves in a cresecendo-
decresendo manner, and rarely lasts longer than 30 seconds; the nystagmus may
have combined torsional and vertical components (if the anterior semi-circular
canal is involved) and the rapid phase usually beats towards the undermost
affected ear, and the nystagmus may change directions when the head is turned to
the opposite side or when the patient sits up (the reversed nystagmus is associated
with less intense vertigo symptoms and a lesser degree of nystagmus) => a key
feature of BPV is that the vertigo and any associated nystagmus (which may be
prominent with initial positioning) fatigues with repeat testing/positioning and
becomes progressively less intense and may disappear temporarily after repeating
the maneuver several times

Differentiating between central and peripheral paroxysmal

positional nystagmus
Appearance Latentcy Duration Fatigability Localisation
Central Pure vertical, Unusual Persistent Unusual Brainstem or
usually cerebellum
downbeat
Peripheral Torsional Usual Brief Usual Posterior or
upbeat or horizontal
 horizontal semi-circular
geotropic canal

- vertigo and nystagmus may also be induced in a patient with BPV affecting the
horizontal semi-circular canals by suddenly turning the patient's head to the
affected side while the patient is lying supine in the horizontal position and observing for
induced vertigo +/- nystagmus => the nystagmus is horizontal, appears after a latent
period of 1 - 10 seconds, and disappears after 1 minute with occasional reversal of the
nystagmus prior to resolution

- head-shaking nystagmus can be induced in some patients with peripheral nystagmus

by asking the patient to close his eyes and then shake his head from side-to-side at a rate
of two cycles per second for about 15 - 30 seconds => after the patient opens his eyes,
nystagmus occurs after a short latent period and is short-lived, and it suggests an
unilateral vestibular disorder

- another bedside clinical test that can suggest peripheral vertigo is the head impulse test

- the test is performed by the examiner turning the patient's head as rapidly as possible ~
15 degrees to one side while the patient continues to fixate on a distant target => the test
is positive (and diagnostic of a peripheral vertigo) if the vestibulo-ocular reflex fails and
the patient cannot continue to fixate on the target, so that he needs to make a rapid eye
movement (a saccade) back to the target after the head impulse is completed

- the head impulse test is only positive in peripheral vertigo and it is only positive when
the head is rapidly turned in the direction of the involved side; the patient should be able
to maintain visual fixation on a distant target when passive rapid rotation to the opposite
normal side is performed

(* see the appendix for further details on the evaluation of nystagmus in vertiginous
patients)

Diagnostic testing

MRI of the head

- the imaging study-of-choice when central vertigo is suspected

- is indicated immediately if :-

 vertigo + profound imbalance and inability to stand

 vertigo + posterior circulation-type neurologic findings
 vertigo + new-onset, severe headache
 vertigo + horizontal nystagmus that changes directions with gaze
 vertigo + any vertical nystagmus
- a MRI can be deferred for 24 - 48 hours if the patient has isolated acute vertigo without
any neurological symptoms/signs, has peripheral-type nystagmus that is suppressed by
visual fixation, and if the patient is only slightly unstable when walking

CT scan of the head

- same indications for testing as for MRI testing

- only indicated if a MRI is not readily available, because it lacks the sensitivity of a MRI
in detecting posterior fossa pathology (it will at least exclude a cerebellar hemorrhage,
even though it may not detect subtle posterior fossa or brain stem lesions or an early
cerebellar infarct)

- fine cuts through the cerebellum should be obtained and clear visualization of the fourth
ventricle is mandatory

- a repeat CT scan (or preferably a MRI) is indicated in 24 - 48 hours to exclude swelling

from a cerebellar infarct if the initial CT scan is negative and the clinical suspicion of a
posterior fossa infarct still exists

Medical decision-making

Acute vertigo of sudden onset

A patient with a sudden headache + acute vertigo + inability to ambulate => a

cerebellar hemorrhage until proven otherwise (even in the absence of other
neurological signs)

- any accompanying altered mental status signifies serious CNS pathology and the
possibility of increased ICP in the infratentorial compartment

- acute vertigo (+/- posterior circulation-type neurological signs) followed by rapid

coma + abnormal breathing patterns + bradycardia/hypertension suggests an acute
posterior fossa bleed (or other rapidly expanding posterior fossa pathology) => rapid
increase in ICP in the infratentorial compartment => brainstem/medulla compression
and/or cerebellar tonsillar herniation

- a patient with acute vertigo, who has associated neurological signs and/or definite
central nystagmus suggestive of an acute central vestibular syndrome, requires a stat
MRI to r/o a posterior fossa hemorrhage or infarct involving the cerebellum or brainstem

- consult a neurologist if a patient with acute vertigo has no associated neurological signs,
but has equivocal, or definite, evidence of a central-type nystagmus
- an inferior cerebellar stroke patient may sometimes not have any associated posterior
circulation-type neurological signs and the nystagmus may only be present in one
direction of gaze - the clinical presentation may therefore closely resemble an acute
peripheral vestibular syndrome

(* a subtle difference is that in patients with peripheral vertigo - the nystagmus, which is
present in only one direction of gaze, intensifies when visual fixation is removed => see
the appendix for further details)

- it is important to search diligently for any subtle clinical clues that could suggest an
isolated inferior cerebellar infarct - i) any axial lateropulsion is towards the side of the
rapid phase of the nystagmus, and ii) the degree of ataxia is slightly greater than would be
expected in peripheral vertigo (in peripheral vertigo the axial lateropulsion is away from
the rapid phase of nystagmus + the ataxia is usually of a lesser degree); iii) cerebellar
infarct patients may also have slightly ataxic pursuit eye movements that may only be
detectable using electro-oculography

- it is sometimes very difficult to properly test for nystagmus or gait ataxia if a patient
with acute vertigo is very symptomatic and unwilling to ambulate => it may better to
defer testing for nystagmus/ataxia and observe the patient in hospital for a number of
hours before deciding whether early neuro-imaging is necessary - based on repeated
clinical evaluations => if the patient still cannot ambulate after a few hours of
observation, he may require a stat MRI to exclude an isolated inferior cerebellar
infarct/hemorrhage that can mimic an acute peripheral vestibular syndrome (especially if
the patient is middle-aged or elderly, and has multiple vasculopathic risk factors for
stroke)

- a patient with typical features of acute peripheral vestibular syndrome, who remains
persistently very symptomatic despite a few hours of IV treatment with droperidol
and/or benzodiazepines, but has only mild imbalance when ambulating => hospital
admission for continued IV therapy => MRI if not significantly improved within 24 - 48
hours

- a patient with typical features of acute peripheral vestibular syndrome can be treated
with anti-emetics (eg. compazine or metoclopramide) +/- a sedative (eg. valium) +/-
neuroleptic agents (eg. droperidol) while in the ED => discharged if symptomatically
improved + able to ambulate + no abnormal neurological signs

- po medications can be continued for symptomatic, outpatient relief => follow-up with
PMD, who can refer the patient prn for ENT evaluation +/- caloric
testing/electronystagmography/audiometry

(* see the appendix for a list of some drugs used in the outpatient therapy of acute
peripheral vertigo)
- a patient with vestibular neuronitis should be warned that a mild positional vertigo or a
vague sense of imbalance may persist for many weeks-to-months

- a patient with a suspected peri-lymphatic fistulae can usually be treated conservatively

=> ENT consultation and outpatient referral (* except when secondary to barotrauma =>
immediate surgical exploration may be indicated)

- a patient with labyrinthine concusion secondary to head trauma may have positional
vertigo that lasts for months => persistent symptoms require ENT evaluation to r/o an
occult peri-lymphatic fistula

Recurrent episodic vertigo

- a patient with recurrent attacks of episodic vertigo lasting a few hours should have
syphilitic or auto-immune labryrinthitis excluded before assuming that the patient may
have Meniere's disease => outpatient workup (including electronystamography +
audiometry) can be performed by the ENT consultant

- an elderly patient with risk factors for cerebrovascular disease + history of episodic
vertigo lasting a few minutes may have vertebro-basilar artery TIA's => consult a
neurologist to decide on inpatient-or-outpatient workup - which may include Doppler
ultrasonography, a MRI and/or angiography

(* it is extremely difficult to make the diagnosis of a posterior circulation TIA if a

multiplicity of associated neurological symptoms does not accompany any short-lived
vertigo lasting < 30 minutes)

- recurrent episodes of vertigo precipitated by exertional straining (or a rapid change in

air pressure), may be due to a peri-lymphatic fistula => refer the patient to an ENT
specialist

Positional vertigo

- defined as short-lived vertigo lasting seconds, and occurring after a latent period when
the head position is changed with respect to gravity

- consult a neurologist if the patient has evidence of a central positional vertigo; a patient
with suspected central positional vertigo may need to be admitted for a neurological
workup

- a patient with suspected benign positional vertigo can be treated by the Epley maneuvre
and then referred to an ENT consultant for further testing (to r/o rare cases of a posterior
fossa tumor or Arnold-Chiari malformation causing central positional vertigo that cannot
be detected by the Dix-Hallpike maneuver in the ED) and further vestibular habituation
therapy (Brandt-Daroff exercises) if still symptomatic and not responsive to a few rounds
of repeat Epley maneuvers
(* see the appendix for details on performing the Epley maneuvre)

- 90 - 95% of patients with BPV have the posterior canal variant, but 5 - 10% of patients
with BPV have the horizontal variant, which provokes vertigo with sudden turining of the
head when lying in bed and not when sitting or looking up; this horizontal variant is
usually unresonsive to the Epley maneuver

- a significant proportion of children with benign paroxysmal vertigo may develop

migraine headaches in later life

Appendix

Evaluation of nystagmus in a patient with vertigo

- it is important to clearly understand the effect of visual fixation on nystagmus testing,

because many cases of nystagmus may be missed or misinterpreted if testing for
nystagmus is only performed using "visual fixation techniques" eg. asking the patient to
fixate on the examiner's finger and instructing the patient to follow the finger as it is
moved from side-to-side

- it is important to check for nystagmus not only when the patient is fixating, but also
when he is not fixating, so that you do not miss subtle clues differentiating peripheral
from central vertigo

Example number 1 - when the nystagmus is present in primary gaze, and in both
directions of gaze

- the direction of the fast phase of the nystagmus is indicated by the direction of the
arrows, and the intensity of the nystagmus is represented by the thickness of the arrows
- in peripheral vertigo, the direction of nystagmus is always in the same direction even if
the direction of gaze changes from left-to-right, while in central vertigo the direction of
the nystagmus can change direction when looking in the opposite direction

- also note that in peripheral vertigo that the intensity of the nystagmus increases when
visual fixation is removed, while the intensity of the nystgamus in central vertigo is
relatively unaffected by visual fixation

Example number 2 - when the nystagmus is only present in one direction of gaze

- note that there is no difference in the direction of the nystagmus, or the intensity of the
nystagmus, when the patient is visually fixating - whether the cause of the nystagmus is
peripheral or central

- note that the only clue to peripheral vertigo can be a slight increase in the intensity of
the nystagmus when the patient is not visually fixating

- is is therefore very important to repeat testing for nystagmus using non-visual fixation
techniques (fresnel lenses or darkened room + patient vaguely staring into the distance
when instructed to look to the left and then to the right) to detect any subtle change in
intensity of the nystagmus - a subtle increase in the intensity of the nystagmus when the
patient is not visually fixating may be the only clue differentiating peripheral from central
vertigo eg. inferior cerebellar infarct

Summary of the clinical features differentiating acute peripheral

vestibular syndrome from acute central vestibular syndrome
Peripheral Central
Onset of vertigo Sudden/gradual Sudden/Gradual
Severity of vertigo Often intense and Less distinct and
disabling disabling
 Pattern of vertigo Paroxysmal, constant, Constant
waxing-and-waning
Vertigo aggravated by Yes No
head or body
movement/position
Associated nausea, Frequent and prominent Infrequent and less
vomiting, diaphoresis severe
Nystagmus type Horizontal or torsional; Horizontal, torsional
or mixed horizonto- or vertical
torsional, but never
vertical or horizontal
Nystagmus direction Unidirectional with fast May be bidirectional,
phase always away from and may change
the affected ear direction with
(irrespective of direction changes in direction
of gaze) of gaze
Nystagmus intensity Intensity decreased or Intensity unaffected
affected by fixation totally suppressed by by visual fixation
visual fixation
Nystagmus intensity Nystagmus intensity may Nystagmus intensity
affected by direction be increased when is usually unaffected
of gaze looking in direction of by direction of gaze
fast phase
Nystagmus Nystagmus decreases or Nytagmus remains
fatiguability disappears with repeat prominent despite
testing repeat testing
Fatigue of vertigo Yes No
symptoms over time
Hearing loss May be present Very infrequent
CNS symptoms/signs Absent Present
Gait Mild-moderate ataxia Moderate-severe
with tendency to fall ataxia with inability
towards one side - to walk, or tendency
opposite to the direction to fall to either side
of the fast phase of
nystagmus

Epley maneuver - Canalith re-postioning maneuver

- this maneuver can be used to treat patients with benign paroxysmal positional vertigo
(BPPV)
- the maneuver is based on the theory that benign paroxysmal positional vertigo
(canalolithiasis) is due the sudden movement of free-floating particles (otoconia) that
accumulate in the posterior semi-circular canal => sudden head movements (looking up,
rolling over in bed, leaning forward) cause the debris to move about en masse in the
posterior semi-circular canal => vertigo lasting a few seconds

- treatment of BPPV can be undertaken in the ED by performing the Epley maneuver as

follows:-

- seat the patient upright on the bed with his head extending over the edge of the bed (as
in the Dix-Hallpike maneuver test) => tilt the patient's head gently 45 degrees towards
the affected side => gently lower the head of the bed so that the patient is lying in the
horizontal position with his head over the edge of the bed - his head should then be about
45 degrees below the horizontal level => wait about 30 - 60 seconds for the patient's
vertigo to subside, and then keep the patient in that position for ~ 3 minutes => turn the
patient's head gently to the midline => wait 30 seconds => turn the patient's head another
45 degrees to the opposite (unaffected) side => wait 30 seconds => let the patient slowly
roll his torso towards that opposite side so that he is lying on that opposite shoulder,
which should enable him to rotate his head another 45 degrees in that opposite direction
so that his face is directed towards the floor => wait 30 seconds for any induced vertigo
to resolve and keep the patient in that position for ~ 3 minutes => slowly bring the patient
back up to the vertical position while he is still lying in that position => then gently turn
his head back towards the midline => when he is sitting upright, tilt the chin down about
30 degrees and keep the patient in that position for a few minutes

- if the patient is very vertiginous during the maneuver, anti-emetics may first have to be
given in order to to successfully complete the maneuver

- the manuever may have to be repeated a few times and the patient should be told to
sleep upright and minimize head movements during the next 24 - 48 hours; the patient
should still expect to have a sense of dysequilibrium for a few days

- a clue to an unsuccessful canolith repositioning maneuver is nystagmus that changes

direction during the maneuver (any nystagmus occurring during the maneuver should be
in the same direction as the original nystagmus, which occurred when the patient was
first placed flat with the affected ear undermost)

(* see section 9 of the emedicine.com chapter on Benign Positional Vertigo to see

photographs of how to perform the Epley maneuver)

Drugs used in the outpatient treatment of acute peripheral vertigo

Scopolamine - 0.5 mg transdermal patch qd
Diphenhydramine - 25 - 50 mg qid
Cyclizine - 25 - 50 mg qid
Meclizine - 12.5 - 50mg tid
Diazepam - 2.5 mg tid
Flunarazine - 10mg qd

Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases

in an ED setting and they should not be regarded as the standard of care. They merely represent the
personal opinions of the author and they should only be used in clinical practice if the reader-user has
substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The
guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical
textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should
particularly confirm all drug doses, their indications and contra-indications, prior to their use.