Lecture 27 - CVD + Pulfrich Flashcards
Origin of acquired colour vision deficiency (CVD)
Can originate anywhere in the visual pathway from photoreceptors to visual cortex
- Ocular pathology
- General pathology
- Brain injury
- Prolonged use of (therapeutic) drugs
Distinguishing congenital from acquired CVD
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
Kollner’s Rule
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
Modern classification of acquired CVD
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.
Type 1
- Red-green
(foveal) cone dystrophies
– Protan like (tri –> mono)
– Reduction / Scotopisation ; Eccentric Fixation
– Loss of VA
– Progression to total colour blindness
Type 2
- Red-Green
Optic nerve disease
Disc abnormalities
Chiasm tumours
– Deutan like (tri –> mono)
– Reduction
– Elevated saturation threshold
– Neutral point at 500nm
Type 3
- 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
S-cone (tritan) defects appearing first
– 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
RG (L/M) defects, but BY defects may also occur:
– Lesions of optic nerve/pathway
– Retrobulbar neuritis
– Leber’s optic atrophy
– Compressive lesions of the optic tract
– Progressive cone degeneration
Mechanism (von Kries) of CVD
- Absorption system
- Alteration system
– Anomalous Trichromacy - Reduction system
– Dichromacy
Clinical Tests:
R/G & Tritan, Diagnosis & grading
– 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
Drug induced CVD
‒ 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
Chromatopsia
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
Assessing acquired CVD with clinical colour vision tests
– 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).
Exact classification of acquired CVD using commonly available clinical tests can be…
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:
Provide comments on Ishihara plates and HRR plates
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
Provide comments on D15 plates and F-M 100 hue test plates
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
Impact of CVD – Driving
- Brake/Rear Lights / Warning Lights – PROTAN DEFECTS
- Traffic signals – DEUTAN DEFECTS
Accident rates of CVD – drivers – mixed evidence
- No greater risk
‒ Psychological adjustment - 1.7x greater risk
– Protans 44/100,000km
– Normals 26/100,000km
Recommendations: - PCV
- DGV
- (No professional DL)
‘Treatment’ of CVD and their disadvantages
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!
When prescribing filter aids it is very important to be aware of the type of CVD and the visual task.
Clinical experience shows that:
– 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)
Pulfrich Effect: Symptoms & Problems
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.
Pulfrich Effect: cause and treatment
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
