Ageing & Eye Movements

Question 1

What do we expect to see as part of normal ageing?

Answer 1

• Wrinkles
• Skin Folds
• Age-related changes to upper lid can lead to ptosis
• Lens opacity – cataracts
• Floaters – PVD
• AMD
• Reduced CS in mid and high spatial frequencies (Pelli Robson may not detect these changes because the frequency between them is lower)

Question 2

What happens to contrast sensitivity as we age?

Answer 2

CS reduces at mid and high spatial frequencies as we age.

Pelli Robson spatial frequencies are lower between them and so may not be as sensitive to picking up CS deficits (Njeru, Osman and Brown, 2021)

Question 3

How are ductions affected in the elderly?

Answer 3

Shechtman et al (2005) - Restrictions in elevation noted

Question 4

What did Chamberlain (1971) find about upgaze in the elderly?

Answer 4

• Longstanding evidence of reduced upgaze with increasing age
• Symmetrical
• Downgaze is normal

Question 5

Why does upgaze reduce with age?

Answer 5

• Disuse or Inferior recti stretched inferiorly as lower lid sags
• Potential it could be EOM fibre degeneration, connective tissue changes/degeneration, midbrain and cranial nerve changes

Question 6

Is there a midbrain reason for changes to vertical eye movements with ageing?

Answer 6

No
Henson, Staunton and Brett (2003) found no significant difference between the young and aged groups in terms of neuronal density and glial cell density in the riMLF (vertical upgaze centre)

Question 7

What did Kowal et al (1998) find about snapped muscles during surgery?

Answer 7

Evidence that snapped muscles during surgery more prevalent in elderly patients

Question 8

What did McKelvie et al (1999) find about ageing of EOM at a microscopic level?

Answer 8

Distinctive progressive changes in the EOM in ageing

Question 9

What did Titova et al. (2024) find out about EOM’s and other muscles?

Answer 9

Highly specialized EOMs fundamentally differ from other muscles

Distinctly different

Compared to other muscles in the body – remain anatomically and functionally intact during ageing

Question 9

What did Clark and Demer (2002) find about EOM muscle paths in the elderly?

Answer 9

LR and MR in older patients are more likely to be in an inferior position and slightly tilted around the globe which can contribute to loss of elevation as acting more are depressors due to the inferior slip (more so LR than MR)

Inferior position of horizontal rectus muscles in older subjects.

Redirect EOM forces from horizontal to downwards.

Difficulty in elevation

Problem with the connective tissue in the orbit is changing which is causing the inferior displacement of the muscle pulleys. This was seen in the MR and LR in the older patients converting horizontal force downwards = upwards limitation. Converts some of the force from the horizontal rectus EOM to infraduction.

Question 10

How are horizontal saccades affected as we age? (Huaman and Sharpe, 1993)

Answer 10

Huaman & Sharpe (1993)
- Accuracy is not affected
- Frequent refixations during saccadic testing

• Saccade Latency
  Increased saccadic latency and more variable saccadic latency potentially thought to be as a result of increased central processing time as several cortical areas are involved in the pathway for saccades. There is degeneration in the ageing brain and increased and more variable latency in the elderly.
• Peak Velocity
  Huaman and Sharpe (1993) found it was not affected but other studies such as Abel et al. (1983) found small reductions with age

Question 11

What is an age-related distance ET?

Answer 11

ET Dist > Nr
- Gradual onset horizontal diplopia in distance
- Concomitant eso deviation
- Broad inclusion criteria
- Mean age of onset = 50 years
- More common in females in 70s
- 1 in 10 new onset strabismus (USA)
- Proposed aetiologies are discussed

Question 12

What is the ageing mechanism similar to and how?

Answer 12

Rutar & Demer (2009)
Similar to myopic ‘heavy eye’

Presentation of ET and/or HoT in the elderly may be explained by
LR-SR band degeneration
i) band thinning
ii) discontinuity
iii) displacement

Connective tissue degeneration
Age-related distance ET and Age-related ET & HoT
Superior transposition of L LR by 1 tendon width.
Ligature of the L LR to the L SR belly

Question 13

How are vertical saccades affected as we age?

Answer 13

Irving & Lillakas (2019)

Accuracy
Amplitude - most saccades hypometric (unless stimulus amplitude <5°)
But other studies (Yang and Kapoula, 2008) found accuracy and binocular coordination of vertical saccades are preserved

Latency
Increased and more variable latency

Peak Velocity
Lower peak velocity

Question 14

Why are saccades thought to be affected in aging (Peltsch et al., 2011)?

Answer 14

Reflexive pro-saccades less affected by ageing suggesting parietal cortex relative unimpaired

Voluntary anti-saccades requiring cognitive input are affected significantly by ageing suggesting vulnerability of the FEFs in the frontal cortex

Corresponds to age related decline in cognitive functions associated with frontal structures, e.g. focused attention, task switching & working memory.

Question 15

What did Nelles et al. (2009) find about saccade induced cortical activation?

Answer 15

Older subjects showed increased activation compared to younger subjects with over-activation in
- Bilateral parietal eye fields
- Right FEF
- Right extrastriate cortex

Question 16

How are smooth pursuits affected in ageing?

Answer 16

Reduces with increasing age including both velocity and latency

Question 17

What has been found about fixation and saccadic intrusions in ageing?

Answer 17

Herishanu and Sharpe (1981)
Higher frequency of SWJ in the elderly – suggested due to nervous system degeneration
Incidence of SWJ similar in younger and older participants
More individual variability in SWJ in elderly participants

Shallo-Hoffman et al (1990)
No difference in SWJs in elderly
Did not find higher frequency

SWJ - Square Wave Jerks

Question 18

How are the cranial nerve nuclei affected in ageing?

Answer 18

Motor neurons in 3rd, 4th and 6th CN nuclei do not decline with age (different to the nuclei of other cranial nerves! Thought to be due to high usage of these) (Sturrock 1989; 1991)

This contrasts with loss of motor neurons from other CN motor nuclei and from the spinal cord where the number declines significantly with age

Possible explanation:
Nuclei supplying EOM are protected from loss of motor neurons by the high level of motor activity in these muscles.

Question 19

What did Sharma (2009) find about CNIII and ageing?

Answer 19

Thirty-eight ON from cadavers aged from 40 post-natal days to 78 years were studied.

• Studied neural & connective tissue organisations of the pre-cavernous part of 3rd CN
• There was a significant increase in the myelin thickness of axons with age.
• Connective tissue gradually increased in later decades and was more pronounced in the eighth decade

Question 20

What are the proposed reasons for morphological changes in CNIII with ageing?

Answer 20

Proposed - cause changes in conduction velocity, resulting in a disruption of the normal timing in neuronal circuits

Whilst studies have found morphological changes in CNIII with ageing (Sharma, 2009) no study has so far shown any relation between ageing changes of the 3rd CN and ocular functions

Question 21

What do we get a higher incidence of in terms of BSV abnormalities in the elderly? Leat et al, (2013)

Answer 21

Leat at al. (2013) found that incrwasing age led to a higher incidence of:
- Strabismus
- Vertical phoria H/Ho
- Near X
- Near E
- Distance E
- Poorer NPC
- Smooth pursuit abnormalities

Question 22

What about excyclotorsion and ageing?

Answer 22

Increasing age – increasing excyclotorsion (slight)
Laterality and gender changes

Proposed reasons:
1) Age-related sagging of LR - ageing and degeneration of LR-SR connective tissue band
2) Reduced phoria adaptation with increasing age

Question 23

Summarise the normal effects of ageing on eye movements

Answer 23

Symmetrical reduction of ductions (upgaze)

Normal fixation
Increased latency of saccades and smooth pursuit
Delays and inaccuracies when using cognitive processing to carry out complex eye movement combinations (anti-saccades)
Voluntary /reflexive eye movements intact

CN, CN nuclei and midbrain intact
Peripheral N structural changes – 3rd CN
EOM structural changes
Muscle pulley location and EOM paths changed
Increased incidence of strabismus