Strategies for Identifying and Treating Unilateral Vestibular Loss

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Strategies for Identifying and Treating Unilateral Vestibular Loss Powered By Docstoc
					  Strategies for Identifying and Treating
   Unilateral Vestibular Loss and BPPV
            Karen Findlater PT

-Dizziness vs Vertigo
-Unilateral Vestibular Loss and Compensation
-Posterior Canal BPPV
-Lateral Canal BPPV
      Canalithiasis vs Cupulolithiasis
-Rx: Particle repositioning maneuvers
            Do pts get both?
  Special thank-you Dr. Lorne Parnes
  for allowing me to use his excellent
          power point graphics


              to Dr. R Ballagh
an artististic ENT resident from our past
   Dizziness vs Vertigo

Not all dizziness is vertigo
 All vertigo is dizziness

  A feeling of lightheadedness, motion sickness, nausea,
  weakness, a fainting feeling
  Often used to describe sense of imbalance, unsteadiness
Many causes:
  Anxiety / panic
  Cardiovascular- arrhythmia, hypotension
  Medications- antihypertensives, anticonvulsants,
  sedatives, hypnotics, others
  CNS disorders- MS, CVA, seizures, migraines, tumour,
  trauma, infection, inflammation

A feeling of movement or spinning when actually still

A feeling of the room spinning around you

Worse with head movements

Associated with nausea / vomiting

Vestibular and CNS disorders
                        Vestibular Anatomy
The Labyrinth
Cupula and Vestibular Hair Cell Physiology
                  Understanding Balance
Normal sensory inputs for motion:
  vision, proprioceptive, tactile, and vestibular

Normal vestibular function:
                    Right                      Left
Head still   _____l l l l___             _____l l l l_____

Turn right   __l l l l l l l l l l l__   ______l l______

Turn left    ______l l_____              __l l l l l l l l l l l___
Vestibular system gives constant monitoring of all head

Visual, somatosensory, and vestibular signals all match

Different sensory inputs are necessary for keeping
balance in different environments

Vestibular connections of concern include
-emotional, anxiety, autonomic response
-nausea and vomiting
-eye movement control
                  Eye Movement Control
           Innervation of the Eye Muscles

VI Abducens- Lateral rectus
IV Troclear- Superior oblique
III Oculomotor- All the rest
Connections of the Semicircular Canals with Muscles of the

Canal              Excitation          Inhibition

Horizontal         ipsi MR             ipsi LR
                   contra LR           contra MR

Posterior          ipsi SO             ipsi IO
                   contra IR           contra SR
Anterior           ipsi SR             ipsi IR
                   contra IO           contra SO
           Normal Eye Movement and VOR

Turn head right
Right vestibular input stimulated
Left is inhibited
Eyes move to left at equal speed to head motion
Keeps object in focus while head moves

If head rotation continued- eyes flick quick to right and slow
    to left as head rotates
Nystagmus is in same direction as head motion ie the side
    that is stimulated
Nystagmus beats away from the side that is inhibited
        Unilateral Vestibular Hypofunction

Sudden loss of peripheral vestibular input unilaterally
causes a sudden onset of vertigo usually associated with
associated with nausea, vomiting and a spontaneous
horizontal nystagmus with the fast phase beating away
from the affected side. In addition, a sense of the body
being pushed to one side and thus an inability to
maintain upright postural control.

As recovery occurs the vertigo will subside but motion
sensitivity predominates. A feeling of dizziness,
unsteadiness and/or loss of visual focus with any head
motion. Occurs during the motion and subsides with
being still.
Patients complain of:

 Difficulty concentrating, memory impairment
 Difficulty focusing, watching motion, reading, computer
 Commotion, noise & crowds bother them
 Some with wt loss from the nausea
 Some with weight gain from the inactivity
    Common Causes of Unilateral Vestibular
Meniere`s disease- a spontaneous increase in pressure
in the vestibular canals causing a temporary loss of
vestibular input on the affected side that lasts for minutes
to hours and recovers. Associated with hearing loss,
tinnitus and aural fullness. Progressive disorder leading
to increased frequency and severity of attacks of vertigo
over decades with eventual hearing loss.

Recurrent vestibulopathy- recurrent severe episodes of
vertigo lasting minutes to hours but not associated with
hearing problems. Cause unknown and treated like
Meniere`s ie low salt diet
Viral labyrinthitis- a viral infection of the inner ear causing
disruption of cochlear and/or vestibular nerve functions.
Usually sudden in onset, and leading to acute vertigo
with or without disruption of hearing, assoc with nausea
and vomiting lasting for several days and improving over
weeks to months with spontaneous recovery of nerve
function (aided by steroids) or with compensation if
permanent impairment occurs

Vestibular neuronitis- inflammation of the vestibular
portion of the vestibulo-cochlear nerve VIII with sudden
onset of vertigo N&V lasting for days and also improving
over months
Acoustic Neuroma (Vestibular Schwannoma)- slow
growing benign tumours that arise from schwann cells of
the vestibular portion of the eighth nerve. Typically pts
present with a gradual hearing loss and/or gradual
dysequilibrium but the surgical removal causes the
sudden and complete vestibular loss. Hearing loss
depends on the surgical approach. Large numbers of pts
seen here who compensate nicely for the vestibular loss
in a couple of months

Ablative procedures for Meniere`s. Labyrinthectomy or
intratympanic gentamicin injections are used to create a
unilateral vestibular lesion to halt to attacks assoc with
Meniere`s disease. Pts are seen to help them
compensate for their unilateral vestibular loss
Sudden loss of vestibular signals on right side:

                              Right              Left
Head still               _____________ dizzy __l l l l_____

Spontaneous horizontal nystagmus beating to left in all 3 directions of
gaze (ie. 1st degree)

In 48 to 72 hours       _____________                ____________

Cerebellar clamp phase, acute compensation, vomiting stops,
nystagmus settles (last to resolve is the horizontal nystagmus in lateral
gaze away from the affected side ie 3rd degree)
Occurs without medication to suppress the good side
Within 6 weeks to two months or more CNS compensation
                       Right             Left
Head still          ___________ not dizzy ___l l l l____

Turn to right       ___________          ___l     l______

Turn to left        ___________           __l l l l l l l l l__

The brain learns to read a new signal for all head motions
So that vision, proprioception, and new vestibular signals
will match again
“Who`s brain will learn this better, someone who practices
or someone who avoids motion?”

In reality CNS plasticity resets the affected side up and
eventually inputs are matched statically and dynamically.

Aided by:
 -practicing motion (habituation), the sooner the better
 -a stable peripheral vestibular lesion
 -healthy, attentive CNS

Hindered by:
 -prolonged immobilization
 -anxiety, meds
 -visual impairment
Vestibular Rehab Promotes CNS Compensation
     Benign Paroxysmal Positional Vertigo BPPV
  Free floating particles (otoconia) (canaliths) dislodged
  from the utricle and settle in the endolymph of the semi-
  circular canals
  Most often the posterior canal (most dependent)
  Also occurs in the lateral canal (less common 30%)
  Posterior canal BPPV can convert to lateral canal with
  particle repositioning maneuver

  Debris or particles adherent to the cupula
  Posterior canal and lateral canal
  More problematic
Canalithiasis and Cupulolithiasis
Usually sudden onset of vertigo (spinning)
Lasting for 10 to 30 seconds (Pts feel its longer)
Coming on after change in position of the head
     lying down
     rolling over
     sitting up from lying
     looking up
     bending over
Associated with nausea, anxiety
Less often vomiting
If severe- motion sensitivity, postural instability, vomiting

Most common peripheral vestibular disorder
Incidence under reported 10-17 per 100,000
Most cases, 50-70%, are primary ie spontaneous,
Higher incidence in women, onset 5th to 7th decade
Secondary causes:
     head trauma (bilateral BPPV)
     vestibular neuronitis (not likely perceived if total loss)
     inner ear surgery
Canal Physiology

Ampellofugal = Movement of the cupula by the endolymph
               fluid away from the ampulla
Ampellopetal = Movement toward the ampulla

In superior (anterior) and posterior semi circular canals:
   -ampellofugal deflection (away) is stimulatory
   -ampellopetal (toward) is inhibitory

In the lateral (horizontal) canal:
   -ampellofugal deflection (away) from the ampulla is
   -ampellopetal (toward) is facilitatory
Dix Hallpike Maneuver
      Testing for BPPV-The Posterior Canal
        Dix Hallpike (Barany) Maneuver
Turn head 45°, quickly lower to 30° below horizontal

Slight delay then an upbeating and torsional (rotatory)
nystagmus toward the ground

So right is counter clockwise, left is clockwise

Particles create an ampullofugal cupular deflection ie

Limited total duration (less than 60 sec)

Sit up, nystagmus reverses, repeat, response fatigues
      Treatment for Posterior Canal BPPV

Reassurance and wait – self limited last months particles
may dissolve, avoid provocative positions

Habituate to the stimulus- old fashioned, unpleasant for
the patient

Particle repositioning maneuvers, very successful except
with cupulolithiasis

Surgical management
-posterior canal occlusion for intractable BPPV
-singular neurectomy (complication of hearing loss)
Particle Repositioning Maneuver
         Modified Epley
Liberatory Maneuver of Semont
              Ineffective Treatment?
Nystagmus reverses to opposite direction either when
sitting up or when roll face toward ground on unaffected
side (if successful stays same direction- ampullofugal)
Might suspect cupulolithiasis-weighed cupula deflects
back in ampullopetal direction and nystagmus is
If inadequate neck ext or done too quickly loose particles
may be falling back into the canal causing ampullopetal
If reversal seen with head to opposite side 45 may have
BPPV in other ear??
                   The Lateral Canal
Cupular barrier is sloped
up, not dependent for
Side lying head on pillow
tilts it perpendicular to the
Short arm (anterior) is
closer to the ampulla
Long arm (posterior) is
closes to the utricle
Particles often in the long
Resolution without Rx
could be expected
                     More Rules
Posterior canal creates torsional nystagmus
Lateral canal creates horizontal nystagmus
Geotropic nystagmus = fast phase toward the ground
Apogeotrophic nystagmus = away from the ground
Remember…. in the lateral canal
-an ampullofugal motion of cupula (away) is inhibitory
-an ampullopetal motion of cupula (toward) is stimulatory
Ewald`s second law of vestibular physiology
-for high accelerations an excitatory stimulus is stronger
than an inhibitory stimulus (because you can only inhibit
so far)
When vestibular input is inhibited horizontal nystagmus
beats with fast phase away from affected side
When stimulated the nystagmus beats toward the
stimulated side
ENG`s COWS= cold opposite, warm same…. cold inhibits
         Testing for Lateral Canal BPPV
Dix-Hallpike test results in horizontal nystagmus

Need to test the Lateral Canal
(Pagnini-McClure`s Manueuver)
-Lie supine on pillow
-Quickly turn head (and body) 90° to one side
-Wait and observe eyes
-Then quickly turn the head 90° to other side

Direction and strength of nystagmus gives information on
type and side of lesion
Horizontal Canal BPPV
            Horizontal Canal BPPV

Canalithiasis- Geotrophic horizontal nystagmus
with lateral head turns to right and left 90°.
Affected side is the side with the strongest

Cupulolithiasis- Apogeotrophic horizontal
nystagmus with lateral head turns to right and
left. Affected ear is the side with the weakest
               Why? Well lets play
 Apogeotrophic Horizontal Canal BPPV

With head turned to side the cupula stays deflected and
many report that the response is intense and sustained
ie not paroxysmal

Newer theories that apogeotrophic variant is caused by
particles in the anterior arm of the lateral canal ie close
to the ampulla
Need to move the particles to the posterior arm then do
the prm with the BBQ roll
               New Table-Lateral Canal BPPV

                 Side of origin and mechanism of BPPV

Intensity of     Apogeotrophic     Apogeotrophic   Geotrophic
                 nystagmus         nystagmus       nystagmus
                 (sustained)       (<1 min)

Stronger on      Right             Right           Left
left side        cupulolithiasis   canalithiasis   canalithiasis
                                   anterior arm    posterior arm
Stronger on      Left              Left            Right
right side       Cupulolithiasis   canalithiasis   canalithiasis
                                   anterior arm    posterior arm
     Rx of Horizontal Canal BPPV Canalithiasis
                 Geotrophic Variant
1. Forced prolonged positioning with affected side
   uppermost- as particles in posterior arm of HC
2. A PRM- Roll through prone away from affected side
   with quick 90° turns pausing for 30 sec. Epley BBQ roll
Why is this good to know?

 Literature reports 6% of cases of posterior
 canal BPPV convert to lateral canal after
 Rx with prm.

 This has happened to my pt.
               Apogeotrophic HC BPPV

Canalithiasis- particles in anterior arm of horizontal canal
  create apogeotrophic horizontal nystagmus. The
  weakest response is the affected side as in

Cupulolithiasis may show a sustained response ie. as long
  as the lateral head turn is maintained
     Rx for Apogeotrophic Variant of HC BPPV

To move the particles from the anterior arm to the posterior
    to converts to the geotrophic variant: Choices!!

1.   Repeated lateral rotations in supine starting with
     affected side down, turn quick 90° up then 90° to
     opposite side. Slowly back to starting position.
     Reported by Nuti 1998
2.   BBQ roll through rapid 90 turns, pause 30 sec, roll
     away from affected side same as for geotrophic variant
3.   Lie on the affected side for 12 hours- float toward the
     posterior arm
                Rx Lateral Canal BPPV
                Apogeotrophic Variant

4. Gufoni et al 1998
a. Sit with head straight
b. Quickly lie onto affected
    side. Wait 1 min after
    nystagmus stops
c. Quickly turn head up 45
    wait 2 min
d. Slowly sit. Repeat if nec
Follow up with treatment for canalithiasis of posterior arm.

    -BBQ roll away from affected side or

    -prolonged positioning with affected side up.
             Rx for Cupulolithiasis

Habituate to weighed cupula
Brandt-Dardoff habituation exercise

1. Vestibular hypofunction (neuronitis) and BPPV
    Treat BPPV then work on compensation. Rules for HC
    likely distorted. Rx the side know to have the neuronitis
    if known
2. Superior Canal BPPV?
    Dix Hallpike results in down beating nystagmus
    right counterclockwise
    left clockwise (as in posterior canal)
    Treat with the Particle repositioning maneuver (Epley)
3. Between Meniere`s attacks?? Any role

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