Transcript Dizziness

Dizziness
Prof. H. Almuhaimed
Objective to be addressed:
Difference between dizziness and
vertigo.
• Diagnostic approach to True vertigo.
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• Characteristics of peripheral vertigo.
• Characteristics of central vertigo.
• Treatment Considerations.
Patients refer to Dizziness as:
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Light headedness
• Faintness
• Giddy
• Imbalanced
• “out-of-it”
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Most dizzy patients can be placed in
to one of four categories:
1- True Vertigo (50%)
2-Pre-syncope:
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Transient sensation that a faint in
about to occur.
• May present as nausea ,weakness, or
change in vision.
• Transient.
3-Dysequilibrium:
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A sensation of imbalance when standing or
walking.
• No illusion.
• No sense of faintness.
4-Vague lightheadedness:
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Holds the reminder of symptoms of
dizziness (which can’t fit to the other
categories)
1.Psychiatric disorders,
2.Hyperventilation syndrome
3.Encephalopathies
What is Vertigo?
True vertigo:
Defined as an “illusion” or
“hallucination” of movement.
• Both vertigo and dysequilibrium
imply a loss of balance, but vertigo
involves a sense of motion.
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How do we maintain
equilibrium?
Visual input
equilibrium
Proprioceptiual
Vestibular input
input
labyrinths.
Anatomy: Semicircular canals
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Semicircular Canals
(SCC)
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Cupula
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Horizontal
Anterior
Posterior
End organ receptors
Endolymph
Anatomy: Utricle
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Utricle
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Connected to SCC
Contains
endolymph
Otoliths (otoconia)
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Calcium carbonate
Attached to hair cells
Macule (end organ)
Vestibular system
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Tells brain which way the head
moves without looking
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SCC: angular acceleration
Utricle: linear acceleration
How can we clinically evaluate
the patient with vertigo?
CN VIII
labyrinth
Cerebellum
(Vestibular portion)
Vertigo
Brainstem
Vestibular
nuclei
Vertigo
Central
peripheral
Key points in History:
•Is true vertigo present?
•Are there associated neurologic symptoms?
•What is the pattern of onset ?
•What is the duration of the symptoms?
•Have there been auditory symptoms?
•Are there other associated symptoms?
•What medications is the patient taking?
•What is the patient’s past medical history?
•Any recent or remote head or neck injury?
Key points in the physical
examination:
•Vital signs
•Ear exam
•Eye exam
•Positional testing
•Neurological exam (including gait)
SPINNED
PERIPHERAL CENTRAL
Sudden (Onset)
Positional
Intensity
Nausea/Diaphoresis
Yes
Yes
Severe
Slow, gradual
No
Ill defined
Frequent
Infrequent
Nystagmus
Torsional/horizontal
Vertical
Ear (hearing loss)
Can be present
Absent
Duration
CNS signs
Paroxysmal
Absent
Carvalho et al.
Constant
Usually present
CTU , Oct, 2004
Peripheral vertigo:
•Approximation 85% of ED patients
with vertigo.
•Due to dysfunction of one of vestibular organs.
•Asymmetry of input
•Sensation of rotation
•Associated with nausea, pallor
and diaphoresis.
Differential Diagnosis
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Benign paroxysmal positional vertigo
(BPPV) (50%)
Vestibular neuritis
Labyrinthitis (suppurative, serous,
toxic, chronic)
Meniere’s disease
FB in ear canal
A cute otitis media
Perilymphatic fistula.
BPPV
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Benign Paroxysmal Positional Vertigo
Age 60- 70 (F:M 2:1)
Head trauma
Characteristic story
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Turn head
After a few seconds delay, vertigo occurs
Resolves within 1 minute if you don’t
move
If you turn your head back, vertigo recurs
in the opposite direction
“BPPV”
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“B” = Benign
Not a brain
tumor
 Can be
severe and
disabling
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“BPPV”
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“P” = Paroxysmal
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Episodic, not persistent
Helpful feature in the differential
diagnosis
“BPPV”
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“P” = Positional
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Occurs with position of head
Turning over in bed
 Looking up
 Bending over
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“BPPV”
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“V” = Vertigo
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An illusion of motion
“The room is spinning”
Other descriptions
Rocking
 Tilting
 Somersaulting
 Descending in an elevator
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Pathophysiology of BPPV
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Otoliths become
detached from hair
cells in utricle
Inappropriately
enter the posterior
semicircular canal
. Parnes LS, McClure JA. Laryngoscope 1992;102:988-92.
Physiology
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Normal situation
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As one turns head to the right
Endolymph moves SCC receptors fire
 “head turning right”
Stop turning head endolymph stops
moving  SCC receptors stop firing 
“head has stopped moving”
Pathophysiology of BPPV
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BPPV
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Stop turning head  otoliths keep
moving  drag endolymph 
receptors continue to fire
inappropriately  “head is still
moving”
Eyes  “head is NOT moving”
Brain  room must be spinning in
the opposite direction
Dix-Hallpike Maneuver
•The diagnosis of BPPV is generally from the
history.
•Can confirm the diagnosis of BPPV
•First described by Dix and Hallpike in 1952.
•Also called the Nylen-Bárány, Bárány,
Nylen, or Hallpike maneuver
Dix-Hallpike Maneuver
They include:
1- Nystagmus
2- Provocative head position
3- Brief latency to symptoms after
change in position
4- Short duration of attack
5- Fatigability of nystagmus on repeat testing
6-Reverse of nystagmus on returning to
upright position.
Lab studies
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In a straightforward case, no lab
studies are needed!
Hemoglobin
Fingerstick glucose
Electrolytes if prolonged vomiting
Epley Maneuver:
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Randomized controlled trials
reported success rates ranging from
44% - 88%
•Froehling et al.
•Wolf et al.
Mayo clin proc
Clin otolaryngol
•Asawarichianginda et al.
Jul 2000
feb 1999
ENT J
Sep 2000
Epley maneuver
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Canalith repositioning maneuver
5 step head hanging maneuver
Moves otoliths out of the posterior
semicircular canal and back into
utricle where they belong
Epley maneuver
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1. Repeat Hallpike
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Previously
performed
diagnostic Hallpike
test tells you the
starting position
(right or left)
Epley maneuver
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2. Turn head 90
degrees in the
other direction
Epley maneuver
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3. Patient rolls
onto shoulder,
rotates head and
looks down
towards floor
Epley maneuver
Epley maneuver
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Repeating the Epley maneuver
Post procedure
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Remain upright for 8-24 hours
The Epley Maneuver
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Contraindications
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Unstable heart disease
High grade carotid stenosis
Severe neck disease
Ongoing CNS disease (TIA/stroke)
Pregnancy beyond 24th week gestation
(relative)
Furman JM, Cass SP. N Engl J Med 1999;341:1590-96
Complications
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Vomiting
Converting to horizontal canal
BPPV
Labyrinthitis and Vestibular
neuronitis
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A cute unilateral loss of peripheral
vestibular function
Associated with vertigo, N/V, and
nystagmus
Worsened by head movement
Occurs in healthy young to middle-aged
adults
Often after respiratory infections
self-limiting
Perilymphatic fistula:
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Due to a traumatic “fistula” at the
round or oval window.
After forceful cough, sneeze, scuba
diving or direct blow to the ear.
Recurrence of vertigo with pneumootoscopy (Hennebert’s sign)
Self-limiting
Meniere’s disease:
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Characterized by triad of:
• vertigo
• tinnitus
• hearing loss (sensorineural)
Chronic relapsing illness (? familial)
Due to a build-up of endolymphatic
pressure in the labyrinth.
Treatment: vestibular suppressants.
Meniere’s disease
Central vertigo
May include disorders with
significant potential morbidity.
 Warrants the initiation of further
work-up.
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SPINNED
PERIPHERAL CENTRAL
Sudden (Onset)
Positional
Intensity
Nausea/Diaphoresis
Yes
Yes
Severe
Slow, gradual
No
Ill defined
Frequent
Infrequent
Nystagmus
Torsional/horizontal
Vertical
Ear (hearing loss)
Can be present
Absent
Duration
CNS signs
Paroxysmal
Absent
Carvalho et al.
Constant
Usually present
CTU , Oct, 2004
Differential Diagnosis:
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Vertebral-basilar circulation
events:
1. Vestibular nuclei (TIA or
stroke)
2. Cerebellar infarction or
hemorrhage
3. Lateral medullary
infarction (Wallenberg’s
syndrome)
4. Vertebral artery dissection
 Migraine
 Post concussive syndrome.
 Tumors (acoustic reuromas)
 Multiple sclerosis
 Infection (encephalitis,
meningitis)
The end