Approach to the dizzy patient
By: Laurence Poliquin-Lasnier
R2 Neurology
What Dizzy means?
• Illusory movement of the environment
(vertigo)
• Lightheadedness
• Imbalance
• Pre-syncope
Questions to ask
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Constant or episodic
Associated symptoms
Gradual vs sudden onset
Aggravating/alleviating symptoms
Duration and frequency of attacks if
episodic
• Triggers
Distinguishing vertigo from other types
of dizziness
• Time course
– Vertigo is never continuous
– The CNS adapts to the defect so that vertigo subsides
over several wks
Distinguishing vertigo from other types
of dizziness
• Provoking factors
– Certain vertigo occur spontaneously, while others
are precipitated by maneuvers that change head
position or middle ear pressure ( coughing,
sneezing, or Valsalva maneuvers)
– Positional vertigo and postural presyncope are both
are associated with dizziness upon standing
– Determine whether dizziness can be provoked by
maneuvers that change head position without
lowering BP or decreasing cerebral blood flow
– Such maneuvers include lying down, rolling over in
bed, and bending the neck back to look up
Distinguishing vertigo from other types
of dizziness
• Aggravating factors
– All vertigo is made worse by moving the head
– Many patients in the midst of a vertiginous attack
are petrified to move
– If head motion does not worsen the feeling, it is
probably another type of dizziness
Key point
• Any type of dizziness may worsen with
position change but disorders such as
benign positional vertigo only occur after
position change
Causes of dizziness
• Peripheral
• Central
• Systemic
Peripheral causes
Hx
Duration
Associated
symptoms
Physical
Vestibular
neuritis/labyri
nthitis
Single prolonged
episode
Days
Nausea, imbalance
Peripheral
nystagmus, +
head thrust,
imbalance
BPV
Positionally
triggered episodes
< 1 min
Nausea, ask for history
of trauma
Positionally
triggered burst of
nystagmus
Ménière
disease
May be triggered
by salty food
hours
Unilateral ear fullness,
tinnitus, hearing loss,
nausea
Unilateral low
frequency
hearing loss
Vestibular
paroxysmia
Abrupt onset,
spont or
positionally
triggered
seconds
Tinnitus, hearing loss
normal
Perilymphatic
fistula
Triggered by sound seconds
or pressure change
or physical strain
Hearing loss,
hyperacusis, ask for
history of trauma
Nystagmus with
change in
pressure
Vestibular Neuritis
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Young adults
Severe vertigo of rapid onset
Nausea, vomiting, imbalance
Symptoms gradually resolve over several
days
• Probably viral etiology
• Generally benign, self-limited course
Benign paroxysmal positional vertigo
• Most commonly recognized cause of vertigo
• Calcium debris within the posterior semicircular canal
(canalithiasis)
• Brief spinning sensation brought on when turning in bed
or tilting the head backward to look up
• Dizziness is quite brief, usually secs, rarely mins
• May be severe enough to halt activity for this duration
• Dix-Hallpike maneuver can provide further evidence of
its presence, but is positive in only 50 to 80% of
patients
• Natural hx of BPPV is one of repeated, brief vertiginous
episodes that are predictably provoked and continue for
wks or months
Ménière’s disease
• Reccurent attacks of vertigo associated with
auditory symptoms (hearing loss, tinnitus, aural
fullness)
• Attacks variable in duration, most last > 20 min
• Severe nausea and vomiting
• Progressive hearing loss
• Bilateral ménière in 1/3 of patients
• Caused by hydrolymphatic hydrops
• Can get acute episodes of falling/being pulled to
the ground caused by acute stimulation of otolith
“otolithic catastrophes of Tumarkin”
Vestibular paroxysmia
• Brief episode of vertigo lasting seconds
• No trigger
• Thought to be 2ary to spontaneous
discharges from damaged VIII cranial
nerve
Vestibular fistula
• Tear or defect in the oval window and/or
the round window (membranes that
separate the middle ear from the fluidfilled inner ear)
• Changes in middle ear pressure will
directly affect the inner ear, stimulating
the balance and/or hearing structures and
causing symptoms
Acoustic neuroma
• Very rare to have vertigo as it is slow
growing so that the CNS has time to
adapt and compensate
• Mostly unilateral hearing loss
Central Causes
Hx
Duration
Associated
symptoms
Stroke/Tia
Abrupt onset
>24hrs vs Brainstem,
minutes
cerebellar
Central nystagmus, focal
neuro signs
Multiple
sclerosis
Subacute
onset
Min-wks
Central, peripheral or
positional nystagmus
Unilateral
vision loss,
diplopia
ataxia
Physical exam
Neurodegen Spontaneous
erative
or positionally
disorder
triggered
Min-hours ataxia
Central/ peripheral
nystagmus, cerebellar,
extrapyramidal, frontal signs
Basilar
migraine
Onset with
typical
migraine
triggers
Seconds
to days
Headache,
Peripheral/ central/
visual aura,
positional nystagmus
photo/phonop
hobia
Familial
ataxia
syndromes
Acutesubacute,
episodic type
with stress,
exercise
hours
ataxia
Central/ positional
Brainstem/cerebellar infarct
• Vertigo is a common symptom in Wallenberg
syndrome/PICA infarct
• Associated with diplopia, horner, crossed pain &
temp loss
• Vertigo may be the only symptom in cerebellar
infarct
• Oculomotor testing can show:
1- Pure unidirectional nystagmus
2- Direction-changing gaze evoked nystagmus
3- Impaired smooth pursuit
4- Overshooting saccades
Multiple Sclerosis
• May be the initial symptom in 5% of patients
• Can get almost any type of vertigo,
including peripheral vertigo when plaque
affects root entry zone of the vestibular
nerve
Neurodegenerative disorder
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Parkinson
Progressive supranuclear palsy
Multi-system atrophy
Progressive ataxia disorders
Dizziness in these patients often better
clarified as imbalance
Posterior fossa structural
abnormalities
• Chiari malformation causes pressure on
cerebellum
• Unsteadiness of gait may be described as
dizziness by patients
• Vertigo is rare
• Posterior fossa tumor (eg medulloblastoma,
gliomas)
Migraine
• Benign recurrent vertigo may be
considered as a migraine equivalent
• With typical migraine triggers
• + family history
• Normal neuro exam
• No progressive hearing loss
Familial ataxia syndromes
• Spinocerebellar ataxia
• Friedreich ataxia
• Episodic ataxia
• + oscillopsia
Systemic causes
• Medications
• Hypotension, presyncope
• Infectious diseases (eg.: syphilis, viral, bacterial
meningitides & systemic infection)
• Endocrine diseases (eg.: DB/hypoglycemia &
hypothyroidism)
• Vasculitis (eg.: collagen vascular disease, giant cell
arteritis, drug-induced vasculitis)
• Hematological disorders
• Hyperventilation, panic attack
On exam:
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Postural vitals
General physical exam
General neuro exam
Neuro-otological exam
Neuro-otological exam
• Ocular motor function testing
– Look for spontaneous nystagmus or saccadic
intrusions
– Nystagmus suggests that the dizziness is vertigo
• Gaze testing
– Look for gaze-evoked nystagmus
– Normal to have non-sustained nystagmus with gaze
greater than 30 degrees
– Vertical nystagmus that increases with lateral gaze
localizes to craniocervical junction and midline
cerebellum
Nystagmus
Feature
Central
Peripheral
Latency
none
2-15 sec
Duration
> 30 sec
5-30 sec
Fatiguability
+/-
++
Vertigo
Usually absent
Usually present
Fixation
No suppression
suppression
Direction
Vertical or horizontal,
direction may change
with head position
Unidirectional,
Horizontal or rotatory,
fast phase toward
normal ear, increased
with gaze in direction of
fast phase
Neuro-otological exam
• Smooth pursuit
– Voluntary mvt of of the eyes used to track
a target moving at a low velocity
– Look for saccadic pursuit
– May occur with early/mild cerebellar
degenerative disorders as the only finding
with minimal ataxia
Neuro-otological exam
• Saccades
– Fast eye mvts used to quickly bring the
image of an object on the fovea
– Shift gaze from one object to another under
voluntary control
– Slowing of saccades = lesion in
pons/midbrain, oculomotor neuron or extraocular muscles
– Overshooting saccades = ocular dysmetria,
sign of cerebellar lesion
– Undershooting saccades less specific and
occur in normal people
Neuro-otological exam
• Optokinetic nystagmus
– Combination of fast saccadic and slow smooth
pursuit observed in N people observing a
moving object
– Patients with severe slowing of saccades will
not be able to generate OKN and will have their
eyes pinned on one side
• Vestibulo-ocular reflex suppression
– Normal individual can fixate his thumb while pt
being turned on himself
– Will elicit nystagmus in pts who have impaired
smooth pursuit
Vestibular nerve exam
• Head thrust test
– When quickly unpredictably turn head of
patient by 30 degree on side, eyes will go
on opposite direction (vestibulo-ocular
reflex) to continue to fixate target
– Abnormal vestibulo-ocular reflex if
observe corrective saccade bringing eyes
back to target after head thrust
– Sensitivity 71% and specificity 82%
Positional testing
• Dix-Hall-Pike
– Burst of upbeat, torsional nystagmus
triggered in patients with BPV by rapid
change from erect sitting to supine headhanging right or left
• Epley manoeuver
– More than 80% effective in treating
patients with posterior canal BPPV
Epley Maneuver
Epley maneuver
• Key feature is the roll-across in the plane
of the posterior canal so that the clot
rotates around the posterior canal and out
into the utricle
Fistula testing
• Test for it if patient reports sound or
pressure induced dizziness
• Pressing or releasing the tragus will
trigger nystagmus
• Other variant with valsava
Gait assessment
• Wide based gait
• Acute vestibular loss may cause the
patient to lean on the side of the affected
ear
Auditory examination
• Otoscopy
• Whisper test (stand behind to prevent lip reading
and occlude/mask the non-tested ear by finger
rub or occluding external auditory canal)
• Whisper 3-6 numbers or letters
• Normal if can repeat 50%
• Weber: lateralizes to ipsi conductive impairment
or contralateral sensorineural
• Rinne: if bone conduction > air conduction = ipsi
conductive hearing loss
Conclusion
• Clarify what dizzy means
• Be patient as history is the most important
part, physical is confirmatory
• Peripheral vs central vs systemic causes
• General physical and neuro exam
• Neuro-otological exam
- Ocular mvts/nystagmus
- Head-thrust
- Dix-Hall pike