Transcript The Dizzy Patient: Diagnosing peripheral vs central lesions

The Vertiginous Patient:
Diagnosing peripheral vs. central
lesions
Natasha Renda
9/23/2009
“This (a patient’s complaint of
dizziness) means that after an
exhaustive inquiry it will still not be
entirely clear what it is that the
patient feels wrong or even less so
why he feels it.”
W.B. Matthews in Practical Neurology
Goals
1. Overview of anatomy and physiology of
vestibulo-ocular system
2. Diagnosing benign positional vertigo
3. Diagnosing acute vestibular syndrome vs.
AICA/PICA stroke
4. Shortcomings of the bedside examination and
imaging
Anatomy
The vestibular system stabilizes
eye position and eye movements
during changes in head position
to maintain focus on an intended
object.
Vestibular Apparatus
Vestibular Apparatus
Ampulla
Three semicircular canals:
sense angular
head movements.
Vestibular Apparatus
Two otiliths: sense linear head movements
and head (body) tilting
1. saccule aligned vertically
2. utricle aligned horizontally
Macula
Vestibular
Nerve
1. Superior division innervation: utricle, anterior
and horizontal SCC’s
2. Inferior division innervation: saccule and
posterior SCC’s
Scarpa’s Ganglion
-Contains cell bodies of superior and inferior
divisions
-Location: internal auditory canals
-Spontaneously fires at 100spikes/second
:Ipsilateral angular head movements
increases firing rate
:Contralateral angular head movements
decrease firing rate
Vascular Supply all from posterior
circulation
1. Vestibular apparatus and
nerve: internal auditory artery
of AICA
2. Vestibular nuclei: branches
of basilar and vertebrals
3. Inferior cerebellum and
flocculonodular lobe:
PICA/AICA
Physiology
Vestibular-Ocular Reflex
Moves eyes in opposite direction
of head movement (rotation or
linear) to maintain an image on
the retina. 3 types of VOR
Want to keep looking at upcoming pontoon boat
1. Boat pitchs up and down and veers left to right
(yaw)
2. Boat moves down river toward other boat
3. Boat tilts left to right
1. Angular VOR:
SCC
Eyes move opposite
to rotation of
head
Pitch: anterior and
posterior canals
Yaw: horizontal
canals
2. Linear VOR: otoliths
Eyes move opposite to
direction of linear head
movement.
Riding elevator: saccule
Riding train: utricle
3. Ocular tilt reflex:
otilith
Eyes and head move
opposite to the tilt of
the body.
Body tilt right: elevates
right eye and
depresses left eye,
leftward head tilt
Loss of canal function causes:
Vestibular Nystagmus
Example: LEFT vestibular neuritis/ left superior
CN8 loss/LEFT HC and AC loss
- Decreased activity from left side of causes slow
phase eye movements to the left 2/2 relative
excitation of firing from the right (healthy) side
- Quick phases generated by burst cells
(nystagmus is named according to quick phase but the
slow phase points toward the deficit)
Clinical
Vertigo
1. symptom: rotation, linear movement, tilt
2. Mechanism: sudden imbalance of neural
activity to vestibular nucleus
3. Localization: labryinth, CN8, vestibular
nuclei, vestibular cerebellum or central
otolith pathways (OR mechanical insult
to inner ear vs central pathways)
4. Signs: N/V, spontaneous nystagmus,
postural instability
Differential using Duration of vertigo
1. Sub-acute attack <3 days
a. vestibular neuritis
b. labyrinthitis
c. Meniere’s disease
d. brainstem CVA: ischemic or hemorrhagic (fatal gastroenteritis)
e. demyelinating
2. Chronic attack >3 days
a. uncompensated unilateral vestibular defect
b. bilateral hypofunction ie. ototoxictiy
c. disequilibrium
d. psychological
3. Episodes
a. seconds: BPPV, orthostatic hypotention
b. minutes: TIA, migraine, seizure, perilymphatic fistula
c. hours: migraine or meniere’s disease
Bedside Examination
Alexander’s Law: peripheral
vestibular nystagmus increases
in intensity when the gaze is in
the direction of the fast phase,
and decreases in intensity when
the gaze is away from the fast
phase
Peripheral Nystagmus
1.
Intensity of vestibular nystagmus and the velocity of
slow phase are increased by removing fixation.
2.
Peripheral nystagmus is unidirectional and central
nystagmus is bidirectional.
To remove fixation
A. Use an opthalmoscope:
1. Observe nystagmus via opthalmoscope
(direction of nystagmus is inverted)
2. Cover and uncover (remove fixation) the
other eye.
 Peripheral disorder IF direction of nystag
and velocity of slow phase are increased
with covering the fixating eye (removing
the fixation)
To remove fixation
B. Frenzel glasses
Summary of nystagmus
1. Pure Vertical or pure torsional: central
2. Combined vertical and torsional:
peripheral or central
3. No nystagmus in vertiginous person:
central
Bedside Examination
1.
Postural instability:
-Peripheral: able to walk, but uncomfortable because leaning
toward side of lesion
-Central: severe, unable to walk without falling
2. Romberg:
-Peripheral: also fall toward side of lesion (instruct not to
compensate)
- Central: variable falling
Bedside Examination
Central localization if other brainstem or
cerebellar signs:
1. CN abnormalities
2. Motor weakness
3. Dysmetria
4. Sensory changes
5. Abnormal reflexes
Other Bedside Examinations
Dix Hallpike test:
Positive in BPPV
Nystagmus begins within 30
sec and lasts <30sec.
If nystagmus persists when
supine, and does not
occur while sitting, suspect
central positional vertigo.
Other Bedside
Examinations
Head Impulse test:
Tests the VOR:
Have patient fixate on your nose.
Rapidly turn patient’s head.
Normal when eyes repeat fixated on nose, but will see
catch up saccade in direction of your nose if abnormal.
Catch up saccades in peripheral etiology but with central
etiologies, test is negative.
Other Bedside Examinations
Smooth Pursuit:
Slowly follow moving target horizontally and
vertically without moving their head
- parietal-occipital cortex, pons, cerebellum
cause catch-up saccades
Further Non-bedside Evaluations
1.
2.
3.
4.
5.
6.
Electronystagmography
Rotary chair
Caloric test
Posturography
Audiometry
Brainstem evoked potentials
Case 1:
55year old woman with spinning sensation
when reaching up for a glass. Ocurrs 23x/week.
Exam: EOMI. Hearing intact. Face symetric.
On Dix Hallpike, vertigo ocurrs and
nystagmus horizontal lasting about
30seconds. Normal head thrust. Able to
walk easily.
Benign Positional Vertigo Furman
et al 1999, NEJM
Benign Positional Vertigo
Symptoms: Episodes provoked by rolling
over in bed, bending over, looking upward
Mechanism: debris within posterior canal
Proceeded by head trauma or vestibular
neuritis
Diagnostics: positive dix hallpike. Negative
neuro exam.
Treatment: Epley maneuver
Who is safe to send home without
further evaluation:
1. Respond well to Epley
2. Normal neurologic exam
3. Classic positive Dix Hallpike test: same
symptoms are provoked by the
maneuver but may or may not provoke
the nystagmus
But the Dix Hallpike has a
positive predictive value of 83
percent and a negative predictive
value of 52 percent for the
diagnosis of BPPV.
Case 2: 70yom hx BPH p/w acute
vertigo.
HPI: While driving, suddenly sensation of being on
a boat. Started about 4 hours ago. Unable to
walk. N/V x2
Exam: right beating nystagmus on rightward gaze
less so on leftward gaze, face symmetric,
hearing intact. No worsening of vertigo or
nystagmus on Dix Hallpike. Head thrust with
catch up saccades. Agrees to stand but gets
very angry with you. Romberg falling toward the
left twice.
Diagnostics: CT shows global atrophy
Clinical exam findings to
distinguish peripheral vs.
central lesions causing vertigo
1. Type of nystagmus
2. Severity of postural stability
3. Presence of any additional neurologic
signs
Hotson, J. Acute Vestibular Syndrome. New England Journal. 1998
Inclusion criteria:
Acute onset vertigo
N/V/retching
Gait instability
One or more stroke RF
Nystagmus
Results:
Neg HIT c/w incipient lateral
medullary stroke (iMRI nl)
Pos HIT: missed some, next
24hr neuro exams
developed my sxs
- Prevalence of dizziness in ER’s: 7.5million
patients/year in USA
- Prevalence of stroke in patients with acute
vestibular syndrome estimated 25%
- 16% AICA strokes can present with a peripheral
presentation with unidirectional nystagmus
- 42% of strokes causing an acute vestibular
syndrome do NOT have obvious central findings
- Head impulse test can also be positive in a
central etiology
Work Up
When to immediately obtain brain
imaging on a pt with vertigo:
• Hx possible for cerebellar hemorrhage
• Exam not COMPLETELY c/w peripheral
vestibular process
• Sudden onset of sxs with stroke risk
factors
• New severe HA along with vertigo
Work Up
When imaging can be delayed 48hours:
a. Isolated acute vertigo
b. Peripheral nystagmus suppressed by
visual fixation, unstable but can still walk
c. Lots improvement in 48hrs (vestibular
neuritis, no need to image)
d. Concurrent acute hearing loss, strongly
peripheral
Work Up
Type of imaging: MRI/MRA. Also
gadolinium with fine cuts through CN8 and
cerebellopontine angle
MRI/MRA within 48hrs with neuro monitoring
in between.
How can a central etiology mimic
a peripheral one?
1. Peripheral labrynth is mimicked by
vestibular nerve or vestibular nucleus
localization
2. Peripheral labyrinth can infarct
because it gets the same blood supply
as the cerebellum (AICA)
Other problems to consider in the
evaluation
1. MRI may be done too early, still negative
DWI
2. DWI is less precise in posterior fossa
(false negatives)
3. A young dizzy person can still have a
vertebral dissection
Dont’ admit someone
with BPV.
Persons with stroke
risk factors with
atypical peripheral
vestibular disorder
findings should have
MRI/MRA.
Thank You
Especially to Dr. Hotson and Dr. Albers
Acknowledgements
Adams and Victor
Blumfeld H. Neuroanatomy through Clinical Cases.
Ganzer …
Hanley K, O'Dowd T. Symptoms of vertigo in general practice: a
prospective study of diagnosis. Br J Gen Pract 2002;52:809-12.
Hoffman RM, Einstadter D, Kroenke K. Evaluating dizziness. Am J Med
1999;107:468-78.
Hotson J, Baloh R. Acute Vestibular Syndrome. NEJM 1998;680-5.
Kerber K, Brown D. Stroke among Patients with Dizziness, Vertigo, and
Imbalance in the Emergency Depeartment: A population based
study. Stroke 2006;37;2484-87.
Newman-Toker D, Kattach J. Normal head impulse test differentiates
acure cerebellar strokes from vestibular neuritis. Neurology 2008;70:
2378-85.
NorrvingB, Magnusson M, Holtas S. Isolated acute vertigo in the
elderly: vestibular or vascular disease? Acta Neurol Scand
1995;91:1:43-48.