Positional and Positioning Tests Nystagmography Flashcards

1
Q

What happens when the head or head and body move from one position to another?

A

The SCC end organ receptors and central vestibular pathways are stimulated in such a way that a compensatory eye movement occurs, helping to maintain fixation on a target during the movement (VOR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens to the cupulae after movement is completed?

A

Should once again be at rest, and no imbalance in the resting afferent activity should occur
In this situation, no nystagmus occurs after the head has—or head and body have—moved from point “A” to point “B”
However, if for some reason an imbalance occurs following the movement, nystagmus will result

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is positioning?

A

Actively moving the patient
Active movement
If the nystagmus occurs as a result of the active motion of the head or head and body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is positional?

A

Static positioning
Positioning the patient and then holding still
If the nystagmus occurs as a result of the new static body position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Can spontaneous nystagmus contaminate positional and positioning tests?

A

Yes
It will usually continue throughout these positions as well, might get worse
The examiner must be aware of the presence of a spontaneous nystagmus when performing this subtest of the ENG/VNG battery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the hallpike maneuver?

A

Positioning test
Test for BPPV - anterior and posterior canal
The patient need not be hooked up to the electrodes for this
The examiner must visualize the patient’s eyes during the procedure using no lenses, Frenzel’s Lenses or Infrared Video
Positive or negative test (you either have nystagmus or you don’t - looking for nystagmus and subjective vertigo)
Looking for rotational movement of the eye - brain tries to match the sense of rotation with the eyes (contracts eye muscles)
Do head roll to assess horizontal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Is hallpike affected by fixation?

A

No
Eyes must remain open

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is hallpike performed?

A

Rapid change from erect torso and head while sitting to a supine head-hanging-left or-right position
The provocative movement is in the plane of the Posterior SCC of the ear on the lower side of the head
The patient is taken rapidly from the sitting to head-hanging position (head turned 45 degrees to each side)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is BPPV?

A

The most common cause of vertigo in the elderly
Caused by canalithiasis or cupulolithiasis of the posterior SCC (or horizontal and anterior SCC) - two variants
Assumed to be the result of displaced otoconia from the utricle settling in the SCC
Unilateral is more common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is BPPV caused by?

A

Can be caused by head concussion, viral labyrinthitis, and occlusion of the vasculature of the inner ear
Most cases it is idiopathic
The majority of people that get it only get it once

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do you diagnose BPPV?

A

Time history of the burst of rotational vertigo and sometimes nausea associated with the typical positioning nystagmus
Both symptoms are induced by rapid head and body movements from the sitting to the head-hanging right or left positions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What do you examine to figure out what type of BPPV they have?

A

Latency
Duration
Linear-rotary nystagmus
Reversal (when the patient returns to the seated position, the vertigo and the nystagmus may reoccur in the opposite direction and less violently)
Fatiguability (constant repetition of the maneuver will result in ever lessening symptoms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does BPPV occur?

A

Inorganic particles (otoconia) detached from the otoconial layer by spontaneous degeneration or head trauma, or viral infection, gravitate to and become settled in the anterior/posterior SCC (canalithiasis) or on the cupula of the anterior/posterior SCC (cupulolithiasis)
The cupula normally has the same specific gravity as the endolymph and is supposed to be a transducer of angular accelerations only
When heavily loaded, it will become sensitive to changes in head position relative to gravity (and create an illusion of rotation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why do most start in the posterior canal?

A

The posterior SCC is situated directly inferior to the utricle when the head is upright
Easy collection bin for detached otoconia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the side-lying maneuver?

A

Done on patient with back or neck issues
Done instead of hallpike
Rotate them down to their side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are positional (static) tests?

A

Supine head center (open and closed)
Supine head turned to right
Supine head turned to left
Whole body lateral right or left (if positions 2 or 3 above demonstrate nystagmus to see if neck torsion is the contributing factor (open and closed))

17
Q

What is the procedure for positional testing?

A

The testing room is dark
Recordings are done for at least 30 seconds in each position (with and without fixation)
The patient is instructed to move their head slowly from one position to another
An Alerting Task is performed by the patient (need to talk to them or tell them to count)

18
Q

What is the criteria for positional nystagmus?

A

It changes direction in any head position, or
It is persistent in at least three head position, or
It is intermittent in all head positions, or
Its slow phase velocity exceeds 6 deg/sec in any head position (could also be 4 degrees/sec)

19
Q

Can positional nystagmus also occur in central pathology?

A

Yes
With the exception of a nystagmus that changes direction within a single position (only peripheral)
Need to consider the central element of it

20
Q

Can positional nystagmus be observed in both peripheral and central vestibular system disease?

A

Yes
Non-localizing finding

21
Q

Do some findings disappear with central compensation?

A

Yes
Spontaneous nystagmus goes away fast
Positional nystagmus and headshake stick around a little longer
Will also see caloric asymmetry
After recovery, spontaneous nystagmus in some patients transiently reverses its direction (Erholungsnystagmus or recovery nystagmus) when the centrally compensated lesion regains function

22
Q

What is periodic alternating nystagmus?

A

This occurs with a variety of cerebellar conditions and is a spontaneous horizontal nystagmus that reverses its direction approximately every 2 minutes
Constant oscillatory motion

23
Q

Is downbeating nystagmus generally central?

A

Yes
And typically cerebellar
When downbeat nystagmus occurs in the primary position of gaze, or more particularly on lateral gaze, it is often accompanied by oscillopsia and postural instability
It is due to a lesional tone imbalance of the vertical VOR

24
Q

What does upbeating nystagmus suggest?

A

Reflects an imbalance of the vertical VOR
Two separate brain stem lesions in the pontomesencephalic junction and in the medulla near the perihypoglossal nuclei are likely to be responsible for this
Can also be a result of vestibular migraine

25
Q

What is positional alcohol nystagmus (PAN)?

A

Specific Gravity Differential
Alcohol is lighter than endolymph, and when blood levels approach 40 mg/dL, alcohol diffuses into the cupula, rendering it lighter than the endolymph
The SCCs are now transformed into gravity-sensitive receptors (not supposed to be)
Nystagmus and vertigo then occur when the subject lies down

26
Q

What are the two phases of PAN?

A

Phase 1 - nystagmus beats toward the undermost ear
With time, blood alcohol diffuses into the endolymph, equalizing its specific gravity to that of the cupula
There is a “silent” intermediate period, beginning between 3.5 hours after cessation of alcohol ingestion, when positional vertigo is absent
Phase 2 - Alcohol selectively diffuses out of the cupula before it leaves the endolymph
This causes the cupula to be transiently denser than the endolymph
Beats to the uppermost ear
Associated with motion sickness
Phase II begins between 5 and 10 hours after cessation of drinking

27
Q

What is central positioning vertigo?

A

When the position of the head is brought to an off-vertical, lateral, or head-hanging position a change in graviceptive (otolithic) input occurs
Positional nystagmus without vertigo is always central: however, the direction of the nystagmus varies
The frequency of central positioning nystagmus is usually low and constant, which distinguishes it from BPPV (also the lack of a latency period after movement into the position)
There is also a lack of fatiguability and habituation

28
Q

What is central positioning vertigo indicative of?

A

Posterior fossa lesion