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נאורו של קליניק > Vestibular Lecture > Flashcards

Vestibular Lecture Flashcards

1
Q

Vestibular system has 3 components:

A
  1. peripheral apparatus (the peripheral sensory apparatus-laberynthe, organs in the middle ear)
  2. the central nervous system processer (Sensory input comes in, areas in the cortex areas of the brain process it and lead to motor output)
  3. Mechanism for motor output (info comes in, is processed centrally and there is a motor output)
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2
Q

Peripheral sensory apparatus:

A

—–Motion sensors in inner ear send info to CNS

—–Head Angular Velocity and Linear acceleration
how fast head is going at different angles, side to side, up and down, forward to back

—–Motion sending to CNS on:

  1. Head angular velocity and linear acceleration
  2. Position of spine relative to head
  3. Spatial orientation WRAT gravity (special orientation of body relative to gravity, if I am upright or flat)
  4. Sense of motion
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3
Q

b. CNS Processor: 3 distinct areas

A
  1. Vestibular Nucleus complex (pons)
  2. Cerebellum (regulate movement, vestibulocerebellum)

Information that comes in combines with other sensory information to estimate head and body orientation

  1. Vestibular Cortex Monitored by cortical processes (“Vestibular Cortex”)-right perisylvian area (doesn’t have anatomical boundries); responding to and acting on input from vestibular apparatus
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4
Q

Mechanism for Motor Output:

A

movement causes motor output, so it is a type of reflex (but not a monosynaptic reflex): ocular muscles, spinal cord

  1. OCULAR MUSCLES and
  2. SPINAL CORD

3 reflexes—(not monosynaptic reflexes but they are movements that result in a specific motor output)[importance: VOR→VSR→VCR]

  1. vestibulo-ocular reflex (VOR):
  2. Vestibulocolic reflex (VCR):
  3. Vestibulospinal reflex (VSR):
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5
Q

vestibulo-ocular reflex (VOR):

A

eye stability with head movement

turn head quickly one way so eye movement equal and opposite to body and/or head movement

in this way we can keep our eyes focused on something even when we are moving

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6
Q

Vestibulocolic reflex (VCR):

A

Stabilization of head on the neck

If eyes fail can substitute with the VCR, if VOR fails can also substitute with VOR

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7
Q

Vestibulospinal reflex (VSR):

A

Compensatory body movements to prevent falls

If someone pushes me left the movement that brings my head back on my body is the VSR

Not only these reflexes but other factors such as proprioception and light touch that help too, but VSR is the main thing that stabilizes the head on the body

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8
Q

Peripheral Sensory Apparatus:

Labyrinth:

Motion sensors that are where? do what? send where?

  1. Combination: of Vestibular input, vision, and proprioceptive input in response to balance tasks (also attention, motor control)
  2. Balance is emergent: depending on the task, different balance apparatuses come in to act on the task
A

made up of Otoliths and Semicircular Canals
Labyrinth = “maze” in inner ear
Oto = ear
Lith = stones

—Motion sensors that are in the inner ear

—detect motion in specific ways

— send information to vestibular nuclei, cerebellum, and the vestibular cortex

Combination: of Vestibular input, vision, and proprioceptive input in response to balance tasks (also attention, motor control)

Balance is emergent: depending on the task, different balance apparatuses come in to act on the task

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9
Q

Balance is emergent:

A

Balance is emergent: depending on the task, different balance apparatuses come in to act on the task

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10
Q

Peripheral Sensory Apparatus: The Labyrinth:

What it is:

A

lies within the inner ear

bony labyrinth—protection and shape

membranous labyrinth

hair cells—lie within the membranous labyrinth

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11
Q

Bony Labyrinth: protection and shape

A

It has 3 semicircular canals
cochlea – hearing

vestibule—central chamber

perilimph—fluid

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12
Q

Membranous Labyrinth:

A

organ
1. Suspended in the bony labyrinth by perilymph and some connective tissue

  1. 5 sensory organs on each side (so that is 10 total): direct link to the CNS through the vestibular nerve
    - —membranous portion of semicircular canals (3 semicurcular canals)

—-otolith organs: utricle and saccule (2 otolith organs)

  1. ampullae: (a sac) widening of the semicircular canals connecting to otolith organs
  2. There is a direct path from the semicircular canals , utricle, and saculae to the CNS through the vestibular nerve (movement picked up by these organs and goes via vestibular nerve to CNS)
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13
Q

ampullae:

what is it

A

(a sac) widening of the semicircular canals connecting to otolith organs

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14
Q

otolith organs:

A

utricle and saccule (2 otolith organs)

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15
Q

5 sensory organs on each side

A

5 sensory organs on each side (so that is 10 total): direct link to the CNS through the vestibular nerve
—-membranous portion of semicircular canals (3 semicurcular canals)

—-otolith organs: utricle and saccule (2 otolith organs)

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16
Q

Hair Cells

where

role

A
  1. Located in each ampullae and otolith organs
  2. Role: convert displacement of head motion into neural firing—head moves, hair cells move, hair cells have connection to VESTIBULAR NERVE and so the movement of the hair cells gets transduced into energy, the energy is sent through the vestibular nerve to CNS
  3. Innervated by afferent neurons located in Scarpas ganglion
  4. when hair cells are bent towards or away from the longest process in the Hair cell, the firing will either increase or decrease
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17
Q

ampullae:

how hair cells work here

A

(a sac) widening of the semicircular canals connecting to otolith organs

Hair cells lie within the CUPULA in the AMPULLAE,

endolymphatic flow across the cupula causes the hair cells to bend, stimulating the hair cells.

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18
Q

otolith organs (utricle and sacule):

how hair cells work here

A

Head movements cause the otoconia (calcium carbonate crystals) to deflect the hair cells of the otoliths (maculae). Otolithes are gravity sensitive !!!

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19
Q

Cupula:

where is it

how hair cells work

A

n the ampulla of each semircular canal
1. Located within the ampulla of each of the semicircular canals

  1. As fluid rushes by the cupula, hair cells within it sense motion, and transmit the corresponding signal to the brain through the VESTIBULAAR CHOCHLEAR NERVE (CN VIII)
  2. HEAD move left, PERILYMPH move right, hair cells deflected by fluid, send the info to sensory nerve
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20
Q

3 Semicircular Canals:

A

angular movement

  1. 2 sets of: (3 on each side = 6 total)
    superior, posterior and horizontal
    *oriented at 90 degrees to each other
  2. respond selectively to head motion along with otoliths (otiliths for linear): ANGULAR VELOCITY, VOR for eye motion, clear vision if head movement
  3. Behave in coplanar pairs (left and right horizontal, left superior and right posterior, left posterior and right superior)
    - —-Stimulation on one side/inhibition on the other side: when angular head motion occurs in the same plane, endolymph in pairs are displaced in equal and opposite directions = excitation on one side
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21
Q

Semicircular Canals respond selectively to head motion along with otoliths (otiliths for linear)

A
  1. responds to angular velocity, provides input about head angular velocity
  2. enables VOR to generate eye movement that matches head movement
  3. allows for clear vision during head motion
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22
Q

Semicircular Canals behave in coplanar pairs (left and right horizontal, left superior and right posterior, left posterior and right superior)

A
  1. They are close to planes of extra-ocular muscles—almost direct relationship of stimulation of hair cells in semicircular canals with corresponding eye motions
  2. Stimulation on one side/inhibition on the other side: when angular head motion occurs in the same plane, endolymph in pairs are displaced in equal and opposite directions—excitation on one side, inhibition on other side
  3. each semicircular canal corresponds to a specific type of motion of the head (ie yaw vs roll vs pitch), can have a pathology in a semicircular canal that will cause a specific issue, this will enable us to localize it
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23
Q

Otoliths:

A

linear movements
1. Utricle and sacculae
Register forces related to linear motion and acceleration

  1. Linear motion
    - —-Vertical motion (up and down head tilts and acceleration) – sacculae
    - —-horizontal motion – utricle
  2. Respond to both linear head movement and static tilt
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24
Q

What does labyrinth interpret and how

A

Labyrinth: interprets the orientation of your head: the brain interprets head orientation by comparing these inputs to each other and to other input from the eyes and stretch receptors in the neck, thereby detecting whether only the head is tilted or the entire body is tipping

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25
Q

Symptoms of vestibular pathology:

A

any of these sx makes us need to question vestibular

  1. Vertigo
  2. Nystagmus
  3. Oscillopsia
  4. Dizziness—vague
  5. Disequilibrium
  6. Motion sickness –if it goes away when you close your eyes it is a hint it is vestibular, it is not due to motion, it is due to inability to keep stable eye position
  7. Nausea and vomiting
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26
Q

Oscillopsia—

A

jumping vision – feels like words jumping on page, even though not in a car (ie malfunctioning VOR)

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27
Q

Disequilibrium

A

—sense of imbalance

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28
Q

Motion sickness

A

–if it goes away when you close your eyes it is a hint it is vestibular, it is not due to motion, it is due to inability to keep stable eye position

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29
Q

Vertigo

what is it

A

if a patient has vertigo then the patient must have vestibular involvement (but if have vestibular involvement don’t have to have vertigo)

  1. only unambiguous symptom of vestibular damage***means vestibular going on

Differentiate from dizziness

Can occur with many other symptoms

Vertigo: can occur with movements that are:

  1. Vertical
  2. Horizontal
  3. Angular
  4. Rotary
  5. Sense of self motion
  6. environmental movement
  7. hallucination of motion: sense of movement occurring when movement is not occurring

Vertigo is not:

  • –*Dizziness:
  • –Lightheadedness, syncope, *orthostatic hypotension:
  • –Disequilibrium: non-specific balance loss
  • –Motion sickness:
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30
Q

Vertigo: can occur with movements that are:

A
  1. Vertical
  2. Horizontal
  3. Angular
  4. Rotary
  5. Sense of self motion
  6. environmental movement
  7. hallucination of motion: sense of movement occurring when movement is not occurring
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31
Q

Vertigo is not:

A

a. *Dizziness: this is not specific, not the unbalanced feeling
b. Lightheadedness, syncope, *orthostatic hypotension: check the medications, hypotension (do you feel lightheaded when stand up quickly, does it feel like the room is moving)
c. Disequilibrium: non-specific balance loss
d. Motion sickness: visual and vestibular mismatch

a. Rule these out
b. Do you get dizzy when stand up
c. Is the room spinning

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32
Q

If a patient has vertigo then the patient

A

if a patient has vertigo then the patient must have VESTIBULAR involvement (but if have vestibular involvement don’t have to have vertigo)

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33
Q

if have vestibular involvement do you have to have to have vertigo?

A

if have vestibular involvement don’t have to have vertigo

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34
Q

Nystagmus:

named what phase

what is it

does it have to be an abnormality

A

b. Nystagmus: named for the fast phase

  1. What it is:
    - Involuntary eye movement
    - Can be physiologic or pathologic
    - Can be stimulated by pushing someone too hard, does not mean abnormality
  2. Phases of Nystagmus:
    - Slow phase: smooth pursuit phase
    - Fast phase: saccadic phase
    - Named for fast phase : ie slow to right and fast to the left named as a left beating nystagmus (or fast clockwise and slow counterclockwise)
  3. Characteristics of Nystagmus: behavior of nystagmus can help diagnose type of vestibular pathology
    - Direction can be vertical, horizontal, angular, rotary, mixed—direction can help us figure out where the lesion or pathology is

-Sustained or unsustained
Similar to clonus that can be sustained or unsustained (and we can thing of the rhythmic beating like spasticity)

-Nystagmus occurs with or without vertigo (we can trigger it in most people if push their VOR) without vertigo is a sign of CNS phenomenon

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35
Q

what is Nystagmus

A
  • Involuntary eye movement
  • Can be physiologic or pathologic
  • Can be stimulated by pushing someone too hard, does not mean abnormality
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36
Q

Phases of Nystagmus:

A
  • Slow phase: smooth pursuit phase
  • Fast phase: saccadic phase
  • Named for fast phase : ie slow to right and fast to the left named as a left beating nystagmus (or fast clockwise and slow counterclockwise)
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37
Q

Characteristics of Nystagmus:

what direction tells us

is it sustained or unsustained

does it occur with vertigo?

A

behavior of nystagmus can help diagnose type of vestibular pathology

-Direction can be vertical, horizontal, angular, rotary, mixed—direction can help us figure out where the lesion or pathology is

-Sustained or unsustained
Similar to clonus that can be sustained or unsustained (and we can thing of the rhythmic beating like spasticity)

-Nystagmus occurs with or without vertigo (we can trigger it in most people if push their VOR) without vertigo is a sign of CNS phenomenon

38
Q

Does nystagmus indicate vertigo?

A

Nystagmus occurs with or without vertigo (we can trigger it in most people if push their VOR) without vertigo is a sign of CNS phenomenon

39
Q

Behavior of nystagmus can help diagnose what?

A

Behavior of nystagmus can help diagnose type of vestibular pathology

40
Q

Benign Paroxysmal Positional Vertigo (BPPV)

A
  1. Most common cause of peripheral vestibular dysfunction*** Usually not appropriately treated by medical community
  2. Most common cause of peripheral vestibular dysfunction
  3. Inappropriate excitation of one or more of the semicircular canals
  4. Easily treated, complete remission is possible and expected
41
Q

Is BPPV inappropriate excitation of one or more of the semicircular canals

A

YES

42
Q

Most common cause of peripheral vestibular dysfunction*

A

BPPV

43
Q

BPPV Diagnosis:

A

Hallpike Dix Manouvre
1. Latency of 1 or more seconds after moved into provoking position

  1. Crescendo and decrescendo of vertigo and nystagmus with duration less than 60 sec
  2. Characteristic nystagmus related to particular canal involvement
  3. Reversal of nystagmus and recurrence of vertigo upon return to sitting
44
Q

Hallpike Dix Manouvre

A

Seated in lognsitting

Rapidly brought down with their head hyperextended and rotation of 45 degrees to a single side—provocative, jolt the semicircular canals

  1. Key things:
  2. Latency of 1 or more seconds after moved into provoking position—latency because it is the otoconia in semicircular canals need to flow through lymphatic fluid and stimulate hair cells, this is not instantaneous and takes a few seconds
  3. Credence and decrescendo of vertigo and nystagmus with duration less than 60 seconds
    - —-Worsening: fluid begin flowing, otoconia bombarding hair cells in cupula
    - —-Better: the otoconia have moved, now there is no new stimulation
    - —-Characteristic nystagmus related to particular canal involvement
  4. Reversal of nystagmus and recurrence of vertigo upon return to sitting —–otoconia and fluid flow in the opposite direction
45
Q

3 key things in hallpike dix

A
  1. Latency of 1 or more seconds after moved into provoking position—latency because it is the otoconia in semicircular canals need to flow through lymphatic fluid and stimulate hair cells, this is not instantaneous and takes a few seconds
  2. Crescendo and decrescendo of vertigo and nystagmus with duration less than 60 seconds
    - —-Worsening: fluid begin flowing, otoconia bombarding hair cells in cupula
    - —-Better: the otoconia have moved, now there is no new stimulation
    - —-Characteristic nystagmus related to particular canal involvement
  3. Reversal of nystagmus and recurrence of vertigo upon return to sitting —–otoconia and fluid flow in the opposite direction
46
Q
  1. Benign:
  2. Paroxysmal:
  3. Positional:
  4. Vertigo
A
  1. Benign: non progressive or life threatening
  2. Paroxysmal: Crescendo/decrescendo (almost like serizure)
  3. Positional: Caused by positions and not movements
  4. Vertigo
47
Q

CC in BPPV

A
  1. Vertigo with sudden head movements usually sitting to lying, lying to sitting, sit to stand and stand to sit
  2. Can cause postural instability when stand up and they can fall
    - —they do fine on the BERG!!!
    - —If someone had a positive hallpike dix and sit to lying causes it, on the berg they will still be fine and wont pick up BPPV
    - —Berg may pick up vestibular disorders, but it wont give you information that would be on the hallpike dix
  3. 2/3 preceded by head trauma, and rest are idiopathic
    - –trauma can cause a jarring of the calcium carbonate crystals from otoliths to semicircular canals
48
Q

how does BPPV pt do on BERG

A
  • —they do fine on the BERG!!!
  • —If someone had a positive hallpike dix and sit to lying causes it, on the berg they will still be fine and wont pick up BPPV
  • —Berg may pick up vestibular disorders, but it wont give you information that would be on the hallpike dix
49
Q

cause of BPPV

A

2/3 preceded by head trauma, and rest are idiopathic

—trauma can cause a jarring of the calcium carbonate crystals from otoliths to semicircular canals

50
Q

BPPV is most common in ____ canal?

A
  1. is most common in posterior semicircular canals
51
Q

Age most common BPPV

A

30-50

52
Q

BPPV : % spontaneous resolution ?

A

50% spontaneous resolution

53
Q

cupulolisthiasis:

A

debris (otoconia) adhering to the cupula of the affected semicircular canal

54
Q

Canalisthiasis

what is it

tx

A

debris (otoconia) floating on the endolymph of the semicircular canal

Canalishiasis makes the canal gravity sensitive –whereas before it was just the fluid now it is the rocks.

Hair cells are stimulated by the otoconia and not the endolymph—(It is a neurological symptom but is is really a mechanical disorder more than a neurological disorder)→

Treatment: move debris out of canal back into the otoliths

55
Q

What does Canalishiasis do to the canal?

A

Canalishiasis makes the canal gravity sensitive –whereas before it was just the fluid now it is the rocks.

Hair cells are stimulated by the otoconia and not the endolymph—(It is a neurological symptom but is is really a mechanical disorder more than a neurological disorder)→

56
Q

Tx Canalishiasis (BPPV)

A

Treatment: move debris out of canal back into the otoliths

57
Q

Epley Maneuver

–which canal

A

BPPV treatment:

aka Canalith Repositioning Maneuver

Works specifically for PSS BPPV (posterior semicircular canal)

Turning of head so that otoconia flows from PSC back into otoliths

58
Q

Hallpike dix maneuver:

which ear is the affected ear?

A
  1. Patient in long sitting
  2. Look up and over L shoulder
  3. Brought rapidly to head hanging position neck extended 20 degrees
  4. Wait 20 to 60 seconds for nystagmus and vertigo (torsional / horizontal)
  5. Nystagmus and vertigo clears return to sitting position
  6. Reversal of nystagmus
  7. Inferior ear is the affected
    ear ***** (ie turn head left so left ear is inferior)

May need 4-5 minutes for nystagmus to clear, 20-40 seconds

59
Q

CRM/Epley:

A

ie left BPPV, after tx tell them not to lie down or get up too fast, no sudden head movements. If some resolution the first time but not complete, generally means need to do it a second or third time. May need a longer period of time. If takes a longer time, possible it is cupulolisthiasis and sticking to the cupula of the affected semicircular canal)

a. Sit upright, legs extended
b. Turn your head to the symptom side at a 45 degree angle and lie on your back (recreating systems like hallpike dix)
c. Remain up to 5 minutes in this position [want otoconia to flow as far through lymphatic fluid as possible]
d. Turn your head 90 degrees to the other side [otoconia still flow, may have some nystagmus]
e. Remain up to 5 minutes in this position
f. Roll your body onto your side in the direction you are facing; now you are pointing your head nose down [nose to floor]
g. Remain up to 5 minutes in this position
h. Bring neck from extension to flexion
i. Go back to the sitting position and remain up to 30 seconds in this position

60
Q

Brandt-Daroff Exercises:

procedure

what theory of BPPV does it address?

A

a. BPPV Home program
b. Habituation vs dislodging debris
c. Adherence issues

d. Brandt Daroff Procedure: more severe procedure (sit→sidelie A→sit→sidelie B)
1. Patient in sitting
2. Rapid movement to sidelying until nystagmus stops, and they stay for 30 second rest, then returns to sitting
3. 30 seconds in sitting
4. moves rapidly to “mirror image” position, waits 30 seconds, then resumes 30 seconds sitting
5. repeated 5-20 times, 3-4 times a day until 2 consecutive days without vertigo

–addresses cupulolisthiasis adherence and rapid movement dislodges it, or person habituates to the vertigo which is possible – debris (otoconia) adhering to the cupula of the affected semicircular canal

61
Q

Brandt-Daroff Exercises:

what theory of BPPV does it address?

A

–addresses cupulolisthiasis adherence and rapid movement dislodges it, or person habituates to the vertigo which is possible – debris (otoconia) adhering to the cupula of the affected semicircular canal

62
Q

Liberatory Maneuvor:

A

VII. Liberatory Maneuvor: For Cupulolisthisasis (severe procedure)

a. Patient moved into provoking side-lying position for 2-3 minutes
b. Patient rapidly moved through sitting position to opposite side-lying position. If no nystagmus, jostle the head. Position maintained for 2-3 minutes.
c. Patient slowly taken into sitting position.

63
Q

Demo: ie had a L positive hallpike dix (+ to the left and – to the right)
a. Hallpike dix;

b. Epley:

A

Demo: ie had a L positive hallpike dix (+ to the left and – to the right)

a. Hallpike dix; Patient in long sitting, Looks up and over left shoulder, Brought rapidly into head hanging position-neck extended ≈20°, Wait 20-60 seconds for nystagmus (torsional/ horizontal)—csescendo and decrescendo, Nystagmus clears, Return to sitting position, Reversal of Nystagmus. Inferior ear is the affected ear
b. Epley: 1.Sit upright. 2.Turn your head to the LEFT side at a 45 degree angle, and lie on your back. 3.Remain up to 5 minutes in this position. 4.Turn your head 90 degrees to the RIGHT side. 5.Remain up to 5 minutes in this position. 6.Roll your body onto your RIGHT; now you are pointing your head nose down. 7.Remain up to 5 minutes in this position. 8-Bring neck from extension into flexion 9.Go back to the sitting position and remain up to 30 seconds in this position.

64
Q

Vestibular neronitis

A

(acute unilateral idiopathic vestibulopathy)—vestibular nerve inflammed

  1. Acute onset of symptoms peaking at 24 hours, lasts 3-4 days
  2. *No hearing loss
  3. Viral infection of middle ear or vestibular nerve
  4. Vestibular symptoms can persist after infection is cleared
65
Q

Labyrinthitis

A
  1. Acute onset of hearing loss, vertigo, Nausea and Vomiting
  2. Often resolves in 3-4 days, but symptoms can persist
  3. *Hearing loss and vertigo can persist
  4. Can be viral or bacterial
66
Q

Meniere’s Disease:

A
  1. Episodic spells of vertigo, hearing loss, tinnitus, “aural fullness”
  2. Pathologic increase in endolymph changes potassium balance between endolymph and perilymph (he thinks a high salt diet is a cause)
  3. Salt restriction, surgery (resections and shunts), vestibular rehab
67
Q

Ototoxicity:

A
  1. Bilateral irreversible vestibular loss—usually to high dose of drug:
  2. Ototoxic drugs (gentamicin, streptomicin) crosses blood perilymph barrier in inner ear
  3. Treatment-increase other balance modalities, vestibulopathy remains –there is damage to both semicircular canals and not side to use for compensation in vestibular rehabilitation
68
Q

Accoustic neuroma:

A
  1. Progressive unilateral loss of vestibular function, hearing, tinnitis
  2. Vertigo present in 20-25% of cases
  3. Schwannoma of vestibular nerve
  4. Respon well to vestibulat rehab
69
Q

Trauma: vestibular issue

A
  1. Dislodging of otoconia
  2. Temporal or labyrinthine fracture
  3. BPPV with other central findings possible [can have central and peripheral]
  4. Central and peripheral vestibular findings possible
70
Q

Central Vestibular Findings:

CAUSE

TX possible?

What is it associated with

Findings

A

Cause: Trauma, demyelination, tumor, ischemia, degeneration of central structures

Treatment: is more difficult but still efficacious

Often associated with multiple co-morbidities

Central Peripheral Findings
1. Vertigo:
Central: doesn’t match nystagmus cannot suppress with fixation

  1. Nystagmus:
    Central: direction changing, either linear or rotary, can be spontaneous

e. Central vestibular pathology
1. can coexist with other balance disorders (ie problems with motor control, proprioception etc, other systems can be involved

  1. Findings can be mixed central and peripheral
  2. Cognitive and behavioral disabilities due to other conditions can complicate vestibular treatment
71
Q

e. Central vestibular pathology
1. can coexist with other balance disorders (ie problems with motor control, proprioception etc, other systems can be involved

  1. Findings can be mixed central and peripheral
  2. Cognitive and behavioral disabilities due to other conditions can complicate vestibular treatment
A

e. Central vestibular pathology
1. can coexist with other balance disorders (ie problems with motor control, proprioception etc, other systems can be involved

  1. Findings can be mixed central and peripheral
  2. Cognitive and behavioral disabilities due to other conditions can complicate vestibular treatment
72
Q

Central Vs Peripheral Findings vestibular

A

Findings
Vertigo:
1. Peripheral: matches nystagmus and suppresses with fixation
2. Central: doesn’t match nystagmus cannot suppress with fixation

Nystagmus:

  1. Peripheral: non direction changing, linear and rotary, due to stimulus
  2. Central: direction changing, either linear or rotary, can be spontaneous
73
Q

Vertigo: central vs peripheral

A

Vertigo:
1. Peripheral: matches nystagmus and suppresses with fixation

  1. Central: doesn’t match nystagmus cannot suppress with fixation
74
Q

Nystagmus: : central vs peripheral

A

Nystagmus:
1. Peripheral: non direction changing, linear and rotary, due to stimulus

  1. Central: direction changing, either linear or rotary, can be spontaneous
75
Q

XI. Testing of vestibular function:

A

a. VORx1: head moves, finger stationary
b. VOR2x2: head moves, finger moves in opposite direction (more provocative)

c. Test vertically, horizontally, and diagonally
d. Test in sitting, standing, walking

Abnormal VOR testing:

  1. Blurry vision/diplopia
  2. Vertigo
  3. Nystagmus
  4. We are trying to recreate original complaint
76
Q

VOR1

A

VORx1: head moves, finger stationary

77
Q

VOR2

A

VOR2x2: head moves, finger moves in opposite direction (more provocative)

78
Q

Abnormal VOR testing:

A
  1. Blurry vision/diplopia
  2. Vertigo
  3. Nystagmus
  4. We are trying to recreate original complaint
79
Q

Dizziness Handicap Inventory (DHI):

A

Dizziness Handicap Inventory (DHI): a form used to evaluate the self-perceived handicapping effects imposed by vestibular system disease.

  1. 25 items subgrouped into three content domains representing functional, emotional, and physical aspects of dizziness and unsteadiness

Respondents choose one of three statements that most applies to them in each section.

0-never, 2-sometimes, 4 always.

The sum of the scores is the total score. Possible score ranges are 0-100

  1. Higher score indicates worse handicap. Subscores for each of the three domains can also be calculated.
  2. Whitney et al (2004) propose that a total score of
    0-30 indicates mild,
    31-60 moderate,
    61-100 severe handicap,
  3. scores relate well to levels of functional balance impairment. (ie similar result to the berg)
  4. Can be used to track progress over time
80
Q

Score on DHI

out of 100

A

Whitney et al (2004) propose that a total score of
0-30 indicates mild,
31-60 moderate,
61-100 severe handicap

81
Q

Frenzel lenses:

A

Used to observe eye movements while minimizing visual fixation during the physical examination of eye movements: [eyes look bigger so we can see the nystagmus better, refraction of lens so patient doesn’t see anything to focus on and cannot suppress with fixation, video feed to see eye on a screen and record it)

82
Q

Computerized Dynamic Posturography (CDP):

A

Subject stands on a forceplate, Responses to various perturbations recorded

Record the force put onto the forceplate, respond to the perturbations

83
Q

Sensory Organization Test (SOT):

A

c. Sensory Organization Test (SOT): Uses CDP to identify abnormalities in patient’s use of the 3 sensory systems that contribute to postural control: somatosensory, visual and vestibular (doesn’t take other systems into account)

Subject stands on a moveable computerized forceplate under 6 different conditions

Three 20 second trials under each of the 6 sensory conditions

CONDITIONS 1-3- support surface fixed –doesn’t move

CONDITIONS 4-6- support surface is “sway referenced”- movement of surface matches movement of the client (if patient heels come up and sway forward the platform moves with you)
-Renders somatosensory cues inaccurate—but it doesn’t do it instantaneously (lag of a few seconds, limits the info you can get from somatosensory cues) so only renders them questionable, only does anterior posterior and not medial to lateral or rotatory

CONDITIONS Vision absent in conditions 2 and 5- visual inputs unavailable

CONDITIONS Moveable visual surround is sway referenced in conditions 3-6 (it moves with patient, only anterior posterior plane)

Constant distance between eyes and visual environment regardless of body sway, making visual cues inaccurate

84
Q

SOT PROS

A

a. RATIO Level Data (excellent data)
b. Baseline normative data (clear numeric picture of how the patient presents)
c. Insurance (reimbursement)
d. In some studies it will pick up subtle changes in balance before other tests do

85
Q

SOT CONS

A

a. Cost
b. Non sensory factors not accounted for
c. Doesn’t test specific task (non-task specific: can do well on the SOT and at certain tasks ie where you need lateral stability, they fall)
d. No better at falls prediction than BBS (BERG BALANCE SCALE)

86
Q

ENG:

A

Electronystagmography(ENG): vestibular testing

  1. Battery of tests looking at nystagmus via EMG recordings from eye movements while subject is subjected to different conditions –put onto extra ocular muscles, muscle activity is recorded
  2. Movements of the eye are recorded during different tracking eye movements and caloric testing
87
Q

Caloric testing:

A
  1. External auditory canal is irrigated by cold or warm water or air: causes firing of the horizontal semicircular canal
  2. COWS rule- Cold Opposite (eye beating in opposite direction), Warm Same
  3. Warm -increased firing of the afferent vestibular nerve. Eyes will turn to the contralateral side with nystagmus to the ipsilateral side
  4. Cold- decreases rate of firing in afferent vestibular nerve. Eyes turn to Ipsialteral side with nystagmus to the contralateral side
88
Q

Vestibular recovery: Theories:

A

a. Adaptation
1. Long term change in response of a system to its input.
2. Stimulus to change is the error signal, provocative testing, the expected response is not the response you want, you need to keep subjecting the person to the stimulus and have their body keep noting the error. We give the patient the VOR training and tell them to keep doing it at a speed, rate, range for mild to moderate symptoms.
3. It must be context specific—need the context and movement that brings on the symptoms in the treatment.

b. Substitution-use of an alternative strategy for lost function. Effectiveness depends on how well the substitution mimics the lost function.
1. Maximization of other modalities (ie vision or proprioception for the other modality).
2. Preprogramming [have the patient learn to anticipate the movement]
3. Smooth pursuit [learn slow and steady eye movements with a steady head]
4. Increasing usage of proprioception and vision

c. Habituation- long term reduction in neurologic response to a noxious stimuli through repeated exposure to that stimuli (repeatedly expose patient to noxious stimuli so that they will find it less noxious)

89
Q

Adaptation

Vestibular recovery: Theories:

A
  1. Long term change in response of a system to its input.
  2. Stimulus to change is the error signal, provocative testing, the expected response is not the response you want, you need to keep subjecting the person to the stimulus and have their body keep noting the error. We give the patient the VOR training and tell them to keep doing it at a speed, rate, range for mild to moderate symptoms.
  3. It must be context specific—need the context and movement that brings on the symptoms in the treatment.
90
Q

Vestibular recovery: Theories:

Substitution

A

Substitution-use of an alternative strategy for lost function. Effectiveness depends on how well the substitution mimics the lost function.

  1. Maximization of other modalities (ie vision or proprioception for the other modality).
  2. Preprogramming [have the patient learn to anticipate the movement]
  3. Smooth pursuit [learn slow and steady eye movements with a steady head]
  4. Increasing usage of proprioception and vision
91
Q

Vestibular recovery: Theories:

Habituation-

A

Habituation- long term reduction in neurologic response to a noxious stimuli through repeated exposure to that stimuli (repeatedly expose patient to noxious stimuli so that they will find it less noxious)

92
Q

VOR Lab

purpose

A

Purpose:

  1. Increase function of VOR by slow graded increases of VOR stimulus
  2. Increase stimulus in four ways: We want mild to moderate symptom of vertigo.
  3. Head shaking speed
  4. Head shaking range
  5. Head shaking direction (vertical, horizontal, angular, rotational)
  6. Increase load of other positions/tasks/distractors
  7. VOR1 vs VOR2

b. Find condition that causes vestibular complaints, Try to recreate sx, Increase intensity as tolerated
c. We want mild to moderate symptoms
d. (sometimes I say close your eyes, that makes recovery faster)

Sample progression Sitting with feet supported, back supported Slow range, slow speed, unidirectional

  1. No sx after 10-20 seconds? Increase head speed,head range, head direction, position, body movement
  2. Sx? Decrease one or more of modalities, ask patient to maintain head shaking so that a mild but tolerable degree of vertigo is maintained. Stop,recover, repeat
  3. Once patient tolerates that level consistently, increase speed, range,direction,position HEP-3-5 reps, 4-5 x a day

Position Changes Sitting supported Sitting unsupported (back, feet) Normal Standing, Standing with narrow BOS, tandem, etc Gait

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