Lecture 27 - CVD + Pulfrich

Question 1

Origin of acquired colour vision deficiency (CVD)

Answer 1

 Can originate anywhere in the visual pathway from photoreceptors to visual cortex
- Ocular pathology
- General pathology
- Brain injury
- Prolonged use of (therapeutic) drugs

Question 2

Distinguishing congenital from acquired CVD

Answer 2

Congenital CVD
– Born with abnormal colour perception
– CVD stable throughout life
– Precise diagnosis and classification
– Identical in both eyes
– Other visual functions normal
– Male/female prevalence different
– Mainly deutan/protan defects

Acquired CVD
– Onset later in life
– Type & severity change
– Difficult to classify – ‘mixed’ responses
on tests
– Often R/L asymmetry
– Other visual functions reduced
– Equal M/F prevalence
– often tritan

Question 3

Kollner’s Rule

Answer 3

Apparently, Kollner actually observed and stated that ‘…B/Y changes first…. R/G is preserved
longer…’, which is in line with a modern, revised version of the rule:
– S cones are physiologically vulnerable and so are more likely to be damaged by receptoral
lesions than L or M cones
– Post-receptoral lesions are more likely to affect both types of cone-opponent neurons: redgreen and blue-yellow

Question 4

Modern classification of acquired CVD

Answer 4

Verriest’s work (Verriest 1963) which assessed spectral luminous efficiency (using laboratory
techniques such as heterochromatic flicker photometry) in colour-normals and patients with
acquired CVD, has led to a more precise classification and description of the characteristics of
acquired CVD.

Question 5

Type 1

Answer 5

• Red-green
  (foveal) cone dystrophies
  – Protan like (tri –> mono)
  – Reduction / Scotopisation ; Eccentric Fixation
  – Loss of VA
  – Progression to total colour blindness

Question 6

Type 2

Answer 6

• Red-Green
  Optic nerve disease
  Disc abnormalities
  Chiasm tumours
  – Deutan like (tri –> mono)
  – Reduction
  – Elevated saturation threshold
  – Neutral point at 500nm

Question 7

Type 3

Answer 7

• Blue-Yellow
  Rod dystrophies/peripheral
  retinal lesions , vascular retinal
  lesions, (senile) maculopathies
  !‘normal aging’ – similar!
  – Tritan like (tri –> di, rarely mono)
  – Reduction or Absorption or Alteration

Question 8

S-cone (tritan) defects appearing first

Answer 8

– Damage due to high light exposure
– Retinal detachment
– Pigmentary degeneration
– Myopic retinal degeneration
– AMD
– Chorioretinitis
– Retinal vascular occlusion
– Diabetic retinopathy
– Papilledema
– Drugs: oral contraceptives, chloroquine

Question 9

RG (L/M) defects, but BY defects may also occur:

Answer 9

– Lesions of optic nerve/pathway
– Retrobulbar neuritis
– Leber’s optic atrophy
– Compressive lesions of the optic tract
– Progressive cone degeneration

Question 10

Mechanism (von Kries) of CVD

Answer 10

1. Absorption system
2. Alteration system
   – Anomalous Trichromacy
3. Reduction system
   – Dichromacy

Question 11

Clinical Tests:
R/G & Tritan, Diagnosis & grading

Answer 11

– Ishihara (6/18)
* Protan/deutan
– HRR (6/60)
* P/D & tritan
– FM 100 Hue
* Age matched
– D15
* Standard/Desaturated
– City Test
* Not suitable!?
– Computerised tests

Question 12

Drug induced CVD

Answer 12

‒ Poor hue discrimination
‒ CVD proportional to VA loss

Dose / time / cumulative effect (examples):
* Dose and time related
– Viagra, alcohol (type 3)
* Cumulative dose effect
– Chloroquine (type3 …1)
* Not dose related
– Digoxin (type 2)
* Hypersensitivity

Question 13

Chromatopsia

Answer 13

Chromatopsia - Classifcation:
Cyanopsia (b), chloropsia (g), xanthopsia(y), erythropsia (r)

Mechanism & Examples
* Scleral discolouration
* Cataract extraction
* Cortical stimulation (drugs)
* Alcohol – cyanopsia
* Adrenalin – chloropsia
* Quinine, atropine - erythopsia
* Sun exposure, toxins & dyes
– Carbon monoxide, arsenic – xanthopsia
* Hysteria

Question 14

Assessing acquired CVD with clinical colour vision tests

Answer 14

– Both eyes must be assessed individually
– Reduced VA and VF defects will limit the use of some tests
– Patients >50 years may present with significant cataract or vitreous haze with will make the detection of acquired type 3 (tritan) defects difficult. Over the age of 75, confusion errors increase considerably due to ‘normal aging’ (Figure 1).

Question 15

Exact classification of acquired CVD using commonly available clinical tests can be…

Answer 15

Exact classification of acquired CVD using commonly available clinical tests can be challenging,
particularly in older patients and patients with ocular pathology that leads to increased prereceptoral light absorption. Generally, to achieve an acceptable degree of diagnostic certainty, a
test battery is required which must include tests for tritan deficiency:

Question 16

Provide comments on Ishihara plates and HRR plates

Answer 16

shihara: 6/18
– Mild defects: increasing number of misreadings
– More severe defects: vanishing plates &
classification plates cannot be seen

HRR plates: 6/60
– Severity of R/G defect can be estimated based on number of grading errors, but classification (type Ior II) usually not possible
– Tritan plates only effective for moderate/severe type 3 defects

Question 17

Provide comments on D15 plates and F-M 100 hue test plates

Answer 17

D15 plates: Large caps can be provided for px with low VA
– Often clear tritan response
– Unreliable when patient has cognitive impairment
[2]

F-M 100 hue test plates:
– Scores must be compared to age-matched
normals
– Very time consuming as binocular testing required

Question 18

Impact of CVD – Driving

Answer 18

• Brake/Rear Lights / Warning Lights – PROTAN DEFECTS
• Traffic signals – DEUTAN DEFECTS

Question 19

Accident rates of CVD – drivers – mixed evidence

Answer 19

• No greater risk
  ‒ Psychological adjustment
• 1.7x greater risk
  – Protans 44/100,000km
  – Normals 26/100,000km
  Recommendations:
• PCV
• DGV
• (No professional DL)

Question 20

‘Treatment’ of CVD and their disadvantages

Answer 20

The common principle behind theses lenses is that they either pass long wavelengths or have spectral transmission curves with notches

• Monocular filter aids
  – e.g. X-Chrom®, Chromagen™
• Binocular filter aids
  – e.g. EnChroma®
• Gene therapy

Disadvantages:
– Colour perception not ‘normal’
– Reduced retinal illuminace
– Effects on BV
* Fusion / Stereopsis
* Asthenopic symptoms
– Pulfrich effect
– Not always permitted!

Question 21

When prescribing filter aids it is very important to be aware of the type of CVD and the visual task.
Clinical experience shows that:

Answer 21

– Patients with mild CVD don’t benefit
– Filters seem to work better for deutan CVD than protan CVD, probably because protans
experience brightness differences naturally (dimming of red)
– Filters do not improve colour naming ability and colour discrimination [3] [4]
– Patients need to understand that apparent ‘improvement’ on isochromatic plate tests does
not equal better colour perception.
– Patients must also be aware of the disadvantages of filter aids (Table 4)

Question 22

Pulfrich Effect: Symptoms & Problems

Answer 22

Moving objects/own movement
* Pouring liquid
* Locating keys into locks.
* Judging the height and width of doors.
* Putting objects in cupboards /drawers
* Position of traffic, kerbs, street lights
* Driving/being driven, cycling
* Navigating crowds
* Pavements, corridors, stairs & escalators
* Tennis, badminton, golf
* Positional errors in embroidery cause
irregular stitching.

Question 23

Pulfrich Effect: cause and treatment

Answer 23

Treatment:
Eliminate latency difference

Cause:
* Optic neuritis (Multiple sclerosis)
* Cataract
* Corneal opacity
* Anisometropic amblyopia
* Anisocoria (induced and traumatic)
* Central serous retinopathy
* Postretinal detachment repair
* Stroke
* Age-related macular degeneration
* Hemianopia
(Eye) conditions