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Binocular vision 2 > Nystagmus > Flashcards

Nystagmus Flashcards

1
Q

what is nystagmus

A

Rhythmic oscillation of one or both eyes

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2
Q

what 3 things can nystagmus be categorized as

A
  • Physiological or pathological
  • Congenital or acquired
  • Manifest or latent
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3
Q

what 4 types of orientation can nystagmus occur in and which is the most common

A

Horizontal, vertical, torsional or a combination

Most commonly horizontal

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4
Q

what type of nystagmus is a combination of horizontal, vertical, torsional a symptom of

A

neurological type nystagmus

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5
Q

what is a manifest nystagmus

A

one that is seen all the time

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6
Q

what is a latent nystagmus

A

one that is only seen when you cover one eye

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7
Q

list the 4 types of physiological nystagmus

A
  • Opto-kinetic (OKN)
    Response to a moving scene (train)
  • Vestibular (VOR)
    Response to rotation of the head (light and dark)
  • End point
    In extreme lateral gaze
  • Voluntary
    5% of the normal population can produce a nystagmus
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8
Q

what is seen in the physiological Opto-kinetic (OKN) type nystagmus

A

a jerk nystagmus, which shows a resetting nystagmus movement e.g. in response to a moving scene (train)

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9
Q

what is seen in the physiological vestibular (VOR) type nystagmus

A

from spinning on a char and when stopping still, the world is still spinning e.g. in response to rotation of the head

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10
Q

list the 3 types of pathological nystagmus

A
  • Benign idiopathic (congenital) - never find the cause
  • secondary to a underlying visual deficit
    Eg albinism = no foveal reflex
    Retinal dystrophies = congenital
  • secondary to neurological deficit
    Intra-cranial lesions = strokes etc, have acquired the nystagmus
    Drug toxicities = alcohol etc
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11
Q

what are the waveforms of nystagmus often only revealed by

A

electronystagmography

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12
Q

what are the 2 forms of waveforms of nystagmus and describe each one

A
  • Jerk
    A slow phase (pathological) and fast phase (refixation); described by direction of saccade e.g. right beat; upbeat; downbeat
  • Pendular
    No fast phase - sinusoidal
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13
Q

which part of the jerk nystagmus revels the direction of the saccade

A

the normal phase which is the fast phase e.g. if looking at the extreme right gaze and the eyes are drifting to the center and then got a quick flick back to the right = a right beating nystagmus

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14
Q

describe a jerk type nystagmus

A

A slow drift off the target, followed by a rapid corrective movement

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15
Q

describe a pendular nystagmus

A

Smooth oscillations = no fast and slow phase and instead just has a gentle sinusoidal pattern which are same at both directions of gaze

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16
Q

if not jerk or pendular, what else can a waveform be and what may a waveform of nystagmus vary with

A
  • May be complex and combinations of jerk/pendular

- May vary with gaze direction

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17
Q

list and explain the 3 terminologies that describes a nystagmus

A
  • Amplitude
    The ‘excursion’ of the nystagmus
    i.e. how far it moves which varies from small excursions to large excursions
  • Frequency
    Number of oscillations per minute
    ‘coarse, medium or fine’
    i.e. if very slow drifting or very fast etc
  • Intensity
    Amplitude x frequency
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18
Q

what is important about the intensity of a nystagmus

A

i.e. the amplitude x frequency
is an important predictor of visual acuity, as everyone with nystagmus has poor visual acuity because the image isn’t always on the fovea

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19
Q

what is the phrase that describes the amount of time the image is on the fovea

A

foveation time

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20
Q

what makes the visual acuity better in terms of intensity of the nystagmus

A
  • a longer foveation time
  • such as slow and small excursions
  • if the amplitude = the longer the time the image is on the fovea, then the better the vision
  • but large amplitudes with slow excursions = less foveating time and worse acuity
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21
Q

what is a manifest type of nystagmus and describe what happens

A

When both eyes are open may increase when one eye is covered, but the nystagmus is always there when both eyes are open

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22
Q

what is a latent type of nystagmus and describe what happens, what is this type of nystagmus also a result of

A
  • only seen when one eye is covered, steady fixation with BEO
  • The result of an early insult to binocular vision
    Eg unilateral cataract, early onset squint
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23
Q

when does Congenital / Early Onset Nystagmus occur

A
  • from 2/3 months and less than 6 months of age

- so not at birth

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24
Q

what are the 2 primary forms of Congenital / Early Onset Nystagmus and what is it not possible to do with these

A
  • sensory deficit nystagmus (SDN)
  • congenital idiopathic nystagmus (CIN)
  • not possible to differentiate SDN/CIN from clinical observation of nystagmus i.e. cant tell if px has got one or another just by looking that them and so they need to have a proper investigation e/h/ from electrophysiology test or a scan, to find out whether its a underlying pathology or if its an idiopathic type nystagmus
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25
Q

what is the aetiology of congenital idiopathic nystagmus (CIN)

A
  • Unknown - maybe something wrong with the neural integrator (the thing that holds the eye movements when gazing)
  • May be x-linked, autosomal dominant or sporadic
  • there is no ocular pathology present and so the diagnosis of this type of nystagmus is only made if nothing else is wrong
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26
Q

what is the aetiology of sensory deficit nystagmus (SDN)and what is needed to be done to find this

A
  • due to early macular deprivatione.g. dense bilateral congenital cataracts, retinal cone dysfunction, albinism (oculo-cutaneous or purely ocular)
  • Careful examination fundus and media and electro diagnostic testing
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27
Q

what is a separate diagnosis from congenital nystagmus and what is this associated with

A
  • Manifest Latent Nystagmus - MLN

- Associated with Early Onset Strabismus & DVD whereby you get a nystagmus as a result of these

28
Q

when is a Manifest Latent Nystagmus - MLN detected and when is it more pronounced

A
  • detected around 2 years of age hence its related to the fact that BVS is disrupted at a very young age
  • more pronounced if 1 eye occluded and in abducted position of gaze
29
Q

describe the waveform in congenital nystagmus and what can cause it to change/vary

A
  • Waveform may change during infancy and may initially present as large roving eye movements, developing into pendular/jerk
  • i.e. may start with babies coming with huge pendular nystagmus who don’t fix and no signs of visual acuity and then later when their visual systems develop, they will develop a jerk nystagmus where they are foveating some of the time and they get better visual acuity
  • Waveform may vary with position of gaze(e.g. pendular in pp, jerk in lateral gaze)
30
Q

what is the direction of congenital idiopathic nystagmus (CIN) nystagmus and in which directions of gaze

A
  • Almost invariably horizontal(may have rotary component)
  • Uniplanar i.e. horizontal in all directions of gaze including vertical i.e. same when looking up and looking down
  • acquired is different as can change when looking up and down in different directions so the va is worse at the direction where the nystagmus is more, because of this they develop a null zone
31
Q

what is the variation of nystagmus with gaze shown by

A

waveforms which increases at a gaze where the nystagmus gets worse

32
Q

what is a null zone

A

Position of gaze of least movement (damping)

33
Q

what will a null zone which is not coincident with pp lead to

A

abnormal head posture (AHP) for best VA

34
Q

what management implications does someone with a large AHP have due to a null zone

A

referral to ophthalmologist

some can do a surgical procedure to get the null position round to the front to get rid of the AHP

35
Q

explain how you will do vision testing on a patient who has nystagmus

A

with and without the AHP

36
Q

what is the average visual acuity of a px with sensory deficit nystagmus (SDN)and congenital idiopathic nystagmus (CIN)

A
  • SDN = 6/60 or less

- CIN = 6/9

37
Q

why is vision testing important in children with nystagmus and what is a good method for vision correction

A
  • as these children also have high refractive errors and get no benefit from their glasses, because if they got a big AHP = they’re looking at the very edge of the lens and not the optical centers of the glasses
  • these patients get better results with contact lenses as they don’t get the same problems as with glasses
38
Q

other than an AHP, what else causes the dampening down of nystagmus, brought about by a null zone and how is this tested

A

when looking at near/close distance i.e. on vergence eye movements with the AHP, and to get the best vision, test with both eyes open as when you cover one eye, the nystagmus gets worse

this is because the MR muscles have a dampening effect, so children get better va’s when they hold the book closer = reduces the nystagmus

39
Q

list how you will do a near vision check when testing a px with nystagmus and what type of results can be expected

A
  • test a patient’s preferred distance (they can achieve N5 in congenital idiopathic nystagmus (CIN))
  • with their AHP and book held close
  • record as e.g. N5 at 8cm etc as this info is important for schooling
40
Q

what can cause a patients nystagmus to get worse than normal and what implications can this have

A
  • when they are tired, anxious or stressed
  • their vision fluctuates throughout the day because of this
  • has implications for driving, e.g. px will be anxious and stressed on driving test day and when asked to read number plate, will not be able to due to decreased visual acuity
41
Q

list 5 other features of congenital nystagmus

A
  • Nystagmus usually similar in both eyes (very rare to see assymetrical type)
  • May increase on occlusion
  • May have associated strabismus
  • May be x-linked, autosomal dominant or sporadic (one off)
  • May have a head nodding (HN)
42
Q

how is head shaking/nodding compensatory for nystagmus, as seen in congenital nystagmus

A

e.g. as they move their head to the left, their eyes go to the right so can make it compensatory where the waveform is reduced

43
Q

what is a rare type of head nodding seen in congenital nystagmus called, at what age does it present, what are the associated signs and what may be the cause of this

A
  • Spasmus Nutans
  • rare condition presenting at 1-2/12 and disappears and resolves by age 3 - self limiting
  • nystagmus, HN, AHP
  • may be dissociated (monocular or asymmetric)
  • tumours around the ON/optic chiasm/3rd ventricle
  • this is the ddx between tumours and something that’s benign
  • so although we know it goes away, we have to refer just incase of a tumour
44
Q

what causes a head nodding to get worse

A

if nervous or stressed

45
Q

which types of patients don’t notice oscillopsia and which ones do and when is it recognized

A
  • not a presenting sign in congenital nystagmus, in adults who has nystagmus as children
  • complaint of oscillopsia strongly suggestive of acquired nystagmus (or voluntary)
  • may be recognized when tired as the nystagmus increases, or in the dark
46
Q

what is another word for voluntary nystagmus and what does this present as

A
  • psychogenic nystagmus
  • presents as acquired nystagmus with oscillopsia and possible head nodding
  • rapid and poorly sustained back-to-back saccades (usually horizontal)
47
Q

how do you confirm that someone has a voluntary nystagmus, and what is it called

A
  • confirm by eye movement recordings

- nystagmography

48
Q

what 6 things are done for the management of congenital nystagmus in childhood

A
  • Refraction and correction even small errors: as this can make a big difference, must be a cyclopegic refraction
  • Accurate assessment of near and distance VA: with and without AHP and with both eyes open
  • Referral to ophthalmologist at initial presentation: i.e. if you are seeing the child for the first time, to rule out an underlying disease
  • Ophthalmologist may arrange paediatric assessment (educational implications) and genetic counselling: may need to do something about their AHP
  • Assessment of consistence and significance of any AHP
  • Monitoring through childhood: in the big stages in their development as when they’re older, they need to move around more e.g. in secondary school and university etc so need help with mobility training
49
Q

list 3 treatment options to reduce the AHP and when will these have little value and at what age should you wait until before carrying out these treatment options

A
  • Surgery to EOMs to move null zone to primary position
  • Prisms to move visual environment to null point
  • Prisms to reduce nystagmus through forced convergence
  • Probably little value if AHP
50
Q

what is the aim of surgery when treating nystagmus

A

moves BEs in direction of AHP to centre the null zone

51
Q

describe how the early surgery for nystagmus in 1953, which was the first operation by Anderson, modified by Gozo and combined into the Kestenbaum procedure was carried out

A

Surgery was done on all 4 horizontal EOMs, with an equal amount of recession and resection:

  • FT or RT
  • RLR 5mm resection and RMR 5mm recession
  • LMR 5mm resection and LLR 5mm recession

had to do surgery on all 4 muscles back in the day, however a 5mm procedure did not have sufficient effect

52
Q

describe how the Park’s modification surgery for nystagmus in 1973 was carried out

A

surgery was done on all 4 horizontal EOMs, but the amount was depending on recession/resection, ME/LR:

  • FT or RT
  • RLR 8mm resection and RMR 5mm recession
  • LMR 6mm resection and LLR 7mm recession
53
Q

list 4 prognosis’s in the results of surgery for nystagmus

A
  • Usually improves but may not abolish AHP: may move null zone area into periphery
  • Effect may not last and may need “re-do” Sx
  • May improve vision: only by making it more comfortable, but visual acuity will still stay the same
  • Most patients will not reach driving standard
54
Q

which surgery causes the AHP to be reduced

A

the Kestenbaum surgery

55
Q

explain how you will prescribe prisms on a patient who has a AHP to the right side to look through their null zone which is on the left side

A

BASE RT BEs to move images to left BO RE, BI LE

= Eyes fixate in left gaze without AHP

56
Q

explain how prisms are prescribed to significantly reduce nystagmus on convergence and in which types of patients will this only really work

A
  • BASE IN BEs to force convergence

- in patients with BSV and adequate motor fusion

57
Q

name an alternative to worked prisms in glasses and the advantage and disadvantage of this

A

Fresnel prisms:

  • is lighter than worked prisms in glasses
  • but will further reduce the vision of patient, who’s vision is already bad to begin with
58
Q

what is the disadvantage of worked prisms in glasses to treat congenital nystagmus, and name some alternatives to this and why

A
  • the lenses are too thick and heavy. they can just be used to show px what its like when null zone is shifted to pp
  • Contact lenses: may be preferable to spectacles in high ametropia or eccentric null zone, and also show nystagmus excursion to slow down = more foveal time and better fixation
  • Biofeedback – may give some voluntary control over nystagmus but no practical long term advantage in vision.
    It is when you attach an electrical signal to the nystagmus so can better adhere to it
59
Q

at what age does someone get acquired nystagmus from

A

anytime after 6 months of age

60
Q

what is the difference in the nystagmus of congenital compared to acquired

A

acquired is usually vertical direction i.e. upbeat and downbeat nystagmus

whereas congenital tends to be horizontal

61
Q

what is a usual aetiology of an acquired nystagmus and why is it important to pick up very quick

A
  • intracranial pathology (e.g. MS, CVA, Meniere’s, tumours, head trauma)
  • so it needs a rapid referral to the right place (which makes it different from congenital)
62
Q

what do patients with acquired nystagmus notice

A
  • the onset
    and
  • oscillopsia

which a congenital nystagmus px won’t complain about

63
Q

list the 4 things than differentiate congenital nystagmus and acquired nystagmus

A
  • History - onset, signs & symptoms
  • Oscillopsia
  • Associated neurological signs
  • Clinical characteristics of nystagmus
64
Q

list the 6 examples os acquired nystagmus

A
  • Upbeat – brainstem lesions
  • Downbeat – cerebellar lesions
  • Abducting nystagmus – INO – lesion MLF(+limited adduction of contralateral eye)
  • Monocular nystagmus – spasmus nutans, tumours optic chiasm/3rd ventricle: = very dissociated i.e. different between RE and LE
  • See-saw - alternating elevation/intorsion one eye and depression/extorsion of the other – chiasmal/parasellar mass lesions
  • Convergence retraction nystagmus syndrome – Parinaud’s/Dorsal midbrain syndrome Gaze-evoked nystagmus
65
Q

list the 4 treatment options for acquired nystagmus

A
  • Removal of cause may help e.g. Arnold Chiari – decompression foramen magnum
  • Drugs may help e.g. baclofen, barbiturates, alcohol & cannabis
  • Surgery to shift null zone – variable success
  • Retroglobal Botulinum Toxin – limited success, useful in non-ambulant patients
66
Q

in which type of patients is the Retroglobal Botulinum Toxin useful in for treating acquired nystagmus and why

A
  • in non-ambulant patients/severely mobility impaired i.e. wheel chair px who mainly spends time watching tv
  • because retro bulbar affects all eye muscles so it stops all eye movements (so are no good for those who are mobile)

Binocular vision 2 (20 decks)

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