As the world Turns
Saleh Fares Aal-Ali
FRCP-R3
Objective to be
addressed:
Difference between dizziness and vertigo.
Difference between dizziness and vertigo.
Diagnostic approach to True vertigo.
Characteristics of peripheral vertigo.
Characteristics of central vertigo.
Treatment Considerations.
Patients refer to Dizziness
as:
Light headedness
Sense of strangeness
Faintness
Giddy
Imbalanced
out-of-it
Most dizzy patients can be placed
in to one of four categories:
1- True Vertigo (50%)
2-Pre-syncope:
Transient sensation that a faint in
about to occur.
May present as nausea ,weakness,
SOB or change in vision.
Transient.
3-Dysequilibrium:
A sensation of imbalance when
standing or walking.
No illusion.
No sense of faintness.
4-Vague
lightheadedness:
Holds the reminder of symptoms
of dizziness (which cant fit to
the other categories)
[Link] disorders,
[Link] syndrome
[Link]
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.
How do we maintain
equilibrium?
Visual input
equilibrium
Proprioceptiual
Vestibular input
input
labyrinths.
Anatomy: Semicircular
canals
Semicircular Canals
(SCC)
Cupula
Horizontal
Anterior
Posterior
End organ receptors
Endolymph
Anatomy: Utricle
Utricle
Connected to SCC
Contains
endolymph
Otoliths
(otoconia)
Calcium carbonate
Attached to hair
cells
Macule (end organ)
Vestibular system
Tells brain which way the head
moves without looking
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 patients past medical history?
Any recent or remote head or neck injury?
Key points in the physical
examination:
Vital signs
Bruits
Ear exam
Eye exam
Positional testing
Neurological exam (including gait)
SPINNED
PERIPHERAL CENTRAL
Yes
Yes
Severe
Frequent
Slow, gradual
No
Ill defined
Infrequent
Nystagmus
Torsional/horizont
al
Vertical
Ear (hearing loss)
Can be present
Absent
Paroxysmal
Constant
Absent
Usually
Sudden (Onset)
Positional
Intensity
Nausea/Diaphores
is
Duration
CNS signs
Carvalho et al.
CTU , Oct, 2004
Case 1
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
Benign paroxysmal positional
vertigo (BPPV) (50%)
Vestibular neuritis
Labyrinthitis (suppurative, serous,
toxic, chronic)
Menieres disease
FB in ear canal
A cute otitis media
Perilymphatic fistula.
BPPV
Benign Paroxysmal Positional
Vertigo
Age 60- 70 (F:M 2:1)
Head trauma
Characteristic story
Turn head
After a few seconds delay, vertigo
occurs
Resolves within 1 minute if you dont
move
If you turn your head back, vertigo
recurs in the opposite direction
BPPV
B = Benign
Not a brain
tumor
Can be
severe and
disabling
BPPV
P = Paroxysmal
Episodic, not persistent
Helpful feature in the differential
diagnosis
BPPV
P = Positional
Occurs with position of head
Turning over in bed
Looking up
Bending over
BPPV
V = Vertigo
An illusion of motion
The room is spinning
Other descriptions
Rocking
Tilting
Somersaulting
Descending in an elevator
Pathophysiology of BPPV
Otoliths become
detached from
hair cells in
utricle
Inappropriately
enter the
posterior
semicircular
canal
. Parnes LS, McClure JA. Laryngoscope 1992;102:988-92.
Physiology
Normal situation
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
BPPV
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-Brny,
Brny Brny,
Brny
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
In a straightforward case, no
lab studies are needed!
Hemoglobin
Fingerstick glucose
Electrolytes if prolonged
vomiting
BHCG
ED Therapy:
1-The Epley Maneuver
First described in 19922
Bedside
Immediate relief
Epley reported an 80% success rate
after a single time and 100% success
rate after more than one session
30%
recurrence rate over a
30-month period.
2.
3.
Epley J. Otolaryngol Head Neck Surg 1992;107:399-404
Lynn S, et al. Otolaryngol Head Neck Surg 1995;113:712-20.
Epley Maneuver:
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
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
1. Repeat
Hallpike
Previously
performed
diagnostic
Hallpike test tells
you the starting
position (right or
left)
Epley maneuver
2. Turn head 90
degrees in the
other direction
Epley maneuver
3. Patient rolls
onto shoulder,
rotates head and
looks down
towards floor
Epley maneuver
Epley maneuver
Repeating the Epley maneuver
Post procedure
Remain upright for 8-24 hours
The Epley Maneuver
Contraindications
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
Vomiting
Converting to horizontal canal
BPPV
ED therapy
2- Vestibular Suppressants:
Meclizine is the most commonly used
(H1 antagonist)
Can significanthy reduce symptoms.
Cohen et at. Arch Nenrol. Aug 1972(RCT)
Dimenhydrinate (Gravol) and diphenhydramine
(Benedryl) have also been used.
Their efficacy is likely mediated by their
anticholinergic activity.
They inhibit muscarinic acetylcholine
receptors involved in feedback from the
brainstem to the vestibular labyrinth.
If N/V
promethazine (phenergan) or
prochlorperazine (stemetil)
(extrapyramidal effect)
Benzodiazepines
generalized inhibition of neural
activity
In a review article:
Authors did not encourage the use
of vestibular suppressants:
suppress the intensity of
symptoms.
but do not reduce the
frequency of attacks.
Furman JM, Cass SP. N Engl J Med 1999;341:1590-96
The Vast majority of peripheral
vertigo can be managed
conservatively.
Surgery for intractable and
incapacitating symptoms.
Labyrinthitis and Vestibular
neuronitis
A cute unilateral loss of peripheral
vestibular function
Associated with vertigo, N/V, and
nystagmus
Worsened by head movement
Occurs in healthy young to middleaged adults
Often after respiratory infections
self-limiting
Perilymphatic fistula:
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 (Henneberts sign)
Self-limiting
Menieres disease:
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.
Menieres disease
When to D/C?
1- Peripheral vertigo.
2- Healthy
3- Help at home.
4- Symptoms controlled.
5- Able to ambulate.
F/U with PMD to arrange
further evaluation if patient
does not improve.
Case 2
Central vertigo
May include disorders with
significant potential
morbidity.
Warrants the initiation of
further work-up.
SPINNED
PERIPHERAL CENTRAL
Yes
Yes
Severe
Frequent
Slow, gradual
No
Ill defined
Infrequent
Nystagmus
Torsional/horizont
al
Vertical
Ear (hearing loss)
Can be present
Absent
Paroxysmal
Constant
Absent
Usually
Sudden (Onset)
Positional
Intensity
Nausea/Diaphores
is
Duration
CNS signs
Carvalho et al.
CTU , Oct, 2004
Differential Diagnosis:
Vertebral-basilar
circulation events:
1. Vestibular nuclei (TIA or
stroke)
2. Cerebellar infarction or
hemorrhage
3. Lateral medullary
infarction (Wallenbergs
syndrome)
4. Vertebral artery dissection
Migraine
Post concussive syndrome.
Tumors (acoustic reuromas)
Multiple sclerosis
Infection (encephalitis,
meningitis)
Neuroimaging in vertigo:
Headache(sudden onset or severe)
Hard neurological findings
No imaging for patients with no
risk factors and exam suggestive
of peripheral vertigo.
Twenty four patients with risk factors
with stroke with history of vertigo
(>48 hrs) and normal neurologic
exam (except nystagemus)
25%
had inferior cerebellar infarction.
Norrving et al. Acta Neurol Scand. Jan 1995
CT vs MRI:
MRI/MRA for vertebrobasilar
disease and cerebellar ischemia .
CT is more sensitive for
hemorrhage
negative CT is not always
reassuring.
Bad Excuses In Court:
1. "I thought the medications
would helpnot cause her to fall
and break her hip.
2. "I know it was vertical
nystagmus, but there were no
other neurological findings so I
assumed it was peripheral
vertigo."
3. "I thought it was obvious that
the patient shouldnt drive."
4. "The vertigo had subsided, so
I thought it was okay for him to
walk to the bathroom.
5. "The patient was too young to
worry about a stroke.
6. "I didnt know that the patient
had decreased hearing.
7. "The CT was normal, so I
thought it was safe to send the
patient home."
8. "The patient came from the
psychiatric hospital, so I
assumed that he was crazy."
The end
