Acquired colour vision deficiencies.
The first article in this series outlined the characteristics of congenital colour vision deficiencies, which are the consequence of an altered genetic code. Acquired colour vision deficiencies can occur in the course of an ocular or systemic disease, or as a side effect of medication or chemical exposure. The assessment of an acquired deficiency will often require a different approach than the assessment of congenital defects. As will become clear in this article, investigations of acquired colour vision defects in the same disease can sometimes yield different results. The discrepancies in the findings may reflect different patient or control groups, or the use of different tests in the assessment of colour discrimination.
Differences between acguired and congenital colour vision defects
There are a number of well-recognised differences between acquired and congenital colour vision defects. The genetic nature of congenital defects means that they are present from birth, are the same in both eyes and are static in nature. Acquired deficiencies appear during a person's lifetime, can occur in one eye only, be more severe in one eye than the other, or can progress or regress depending on progression or regression of the disease. Other signs, such as reduced visual acuity (VA) or visual field defects, may accompany acquired deficiencies but other aspects of visual function are not altered in congenital dichromats and anomalous trichromats.
The prevalence of congenital deficiencies is greater in males than in females, whereas the prevalence of acquired deficiencies will be the same in both, and a discrepancy will only be seen if there is higher prevalence of the particular causative disease in males or females. Most congenital defects affect colour discrimination along the red-green axis whereas most acquired defects impair tritan discrimination.
Classification of acquired deficiencies
It was recognised in the 17th Century that colour vision deficiency could occur as a result of illness or any treatment received for it. (1) An acquired colour vision deficiency can reflect a problem that occurs anywhere along the visual pathway where information about colour is processed, from the photoreceptors to the cortex. Changes to the optical media can also affect colour discrimination. An acquired deficiency may exhibit the characteristics of more than one congenital deficiency. In 1912, Kollner described acquired colour deficiency in the following way (cited by Marred (2)).
"'Blue--yellow blindness': Blue and yellow change their appearance first, green and red are longest seen unchanged and most of the other hues approach these two colours. The acquired 'blue-yellow blindness' especially develops in diseases of the retina. Only in combination with 'progressive red-green blindness' does it lead to total colour blindness."
"'Progressive red-green blindness': The colour vision is totally disturbed. The blue-yellow vision is changed too, but the deterioration is most striking in the region of red and green. This type of disturbance can especially be found in diseases of the conduction pathways, reaching from the inner layers of the retina to the cortex."
The above is often interpreted as 'optic nerve head diseases result in red-green defect whereas diseases of the retina cause blue-yellow defects', and is referred to as "Kollner's rule". This interpretation is not strictly correct, as Kollner's definition of colour defects seen in diseases of the conductive pathway also mentions the presence of a blue-yellow defect.
Verriest (3) proposed a classification system that identifies three types of acquired colour vision defects in which a main axis of confusion can be identified. Types 1 and 2 are red-green deficiencies. Type 1 exhibits protan discrimination characteristics with an altered protan-like spectral luminosity function, in which the wavelength of maximum sensitivity is shifted towards shorter wavelengths. Type 2 is a deutan-like acquired deficiency with a normal peak of the spectral luminosity function. Type 3 is a tritan-like defect, sometimes also referred to as a blue-yellow defect. It may be accompanied by a shift of maximum luminance sensitivity to shorter wavelengths (pseudoprotanomaly). Verriest also recognised that sometimes there is no prominent axis of confusion in an acquired colour vision deficiency.
Current investigations of acquired colour vision deficiencies often concentrate on the sensitivities of the two chromatic systems and therefore only a red-green vs. tritan (blue-yellow) distinction may be possible. Acquired colour vision defects are often tritan in nature. This predominance has been attributed to the susceptibility to damage of the short wavelength sensitive cone (S-cone) pathway (eg the cones themselves, their connections, or the ganglion cells to which they connect) by, for example, high intraocular pressure (IOP) (4) or hypoxia. (5) It has also been suggested that the scarceness of the S-cones and cells involved in the processing of their signals can lead to an earlier detection of the defect in this subsystem of colour vision. (6)
Testing for acquired deficiencies
A battery of tests will often be needed to characterise an acquired colour vision defect. Since an acquired colour deficiency can occur in one eye, or be more severe in one eye, testing must be conducted monocularly. Acquired deficiencies can be red-green or tritan in nature and it is therefore important to include tests that can detect both types of defects. Acquired deficiencies do not always follow the same well-defined patterns as congenital deficiencies. Therefore a test that can show the mixed defects may be beneficial (see article two in this series, OT October 23 2009, for full details of individual colour vision tests). Ideally, the test will not only identify the presence of a colour vision defect but will also grade its severity.
[FIGURE 1 OMITTED]
The Ishihara test will identify Type 1 and Type 2 red-green deficiencies and therefore cannot be used as a standalone test in the assessment of acquired colour deficiencies, which are often tritan in nature. The characteristics of the responses may change with the severity of the defect, from mis-readings to not being able to read any of the plates of the test. (7) The Hardy, Rand and Rittler (HRR) plates (Figure 1) may be more useful as tritan plates are also included in the test and the severity of the defects can be graded. (8) The City University tritan test can detect tritan defects and identify those in whom the defect is severe. (7)
The Farnsworth-Munsell (FM) 100 Hue test has been a popular choice in the assessment of acquired colour deficiency. In this test, the assessment is not confined to a particular direction in colour space, and quantitative results can be obtained. However, care must be taken when analysing the results as the error score is affected by the patient's age (3) and can also be influenced by other factors such as illuminance (9) and practice. (10) In some patients with an acquired colour deficiency, the error scores can be high and it may be difficult to define an axis of confusion from the polar diagram. Birch and Dain (11) proposed an averaging method that makes it easier to classify a defect in the presence of poor hue discrimination.
The Farnsworth D15 test may also be useful in the assessment of an acquired deficiency, especially as the examination is a lot faster than with the FM 100 Hue test. Desaturated versions of the tests are more difficult than the standard, and may be needed in some cases to reveal the impairment. The results of this group of tests can then be used to grade the severity of the defect.
An evaluation of the Rayleigh and Moreland matches in an acquired deficiency may reveal an enlarged matching range and a shifted midpoint. (7,12) The evaluation of both equations will often be needed to classify the defect. (13)
Computerised colour vision tests are an excellent choice when assessing acquired colour deficiencies as colour discrimination can be probed along a number of directions in colour space. These methods employ techniques used in visual psychophysics to measure colour discrimination thresholds. When a full colour discrimination ellipse is not required, thresholds along the protan, deutan and tritan confusion lines will be of interest.
Acquired colour vision defects may be accompanied by reduced VA or visual field defects. The impact of these on colour vision test performance must therefore be considered in patients suspected of having an acquired colour deficiency. However, colour vision assessment may still be possible, if an appropriate test is selected. For example, a study that used refractive blur to reduce VA, indicated that the HRR plates can be successfully administered with a logMAR VA of 1.10 and the D15 test with a logMAR VA of 1.40. (14) An enlarged version of the D15 test may also be a suitable option. In studies that use computerised methods of assessment, the stimuli can be specifically designed to take into account the patient's reduced VA. (15)
Current research tends to evaluate not only whether a disease process or medication alters colour discrimination, but also whether any changes in colour discrimination can predict the progression of the disease or be used as a sign of toxicity. The non-invasive nature of colour vision testing makes it particularly attractive for these purpose.
Age-related changes of the crystalline lens
Age-related changes alter the transmittance properties of the crystalline lens. The optical density of the lens increases with age, leading to an increase in the absorption of short-wavelength (blue) light. (16) This can give rise to a tritan-like defect.
The total error score of the FM 100 Hue test deteriorates with age from about the third decade of life (Figure 2). (3,17) An analysis of partial errors that considers errors made along the red-green (RG) and blue-yellow (BY) axis has shown that errors along both axes contribute to the increase in the score, with a greater contribution from the BY scores. (16,17) However, the deterioration of the score can only be partially attributed to lens yellowing. (17) An investigation of the error scores on the FM 100 Hue test showed that simulation of lens yellowing in young subjects did not lead to the same lowering of scores as was observed in older subjects with a naturally yellowing lens. The authors attributed the difference to other factors, such as pupil size, macular pigment, illumination, and iris colour. Nevertheless, when the FM 100 Hue test is used, it is important that age-related changes are taken into account.
The effects of increasing lens density can also be seen in colour matching. As the density of the lens increases, the Rayleigh match shifts towards the green end of the spectrum and the Moreland match towards the blue end. (18) In some groups of patients with an ocular or systemic disease, the age related changes in the crystalline lens are more advanced than in age-matched controls.
It is therefore more appropriate to compare the results of those patients to the results of a group of lens-density matched rather than age-matched controls. Alternatively, age norms from a group at least 10 years older could be used. (7) This practice helps to ensure that if a defect is found, especially of tritan discrimination, it is one actually caused by the disease under investigation.
Ocular and Systemic Diseases
Research on colour vision in diabetes tends to concentrate on two issues; firstly on characterising colour discrimination before any signs of diabetic retinopathy are visible, and secondly on analysing colour vision in patients with retinopathy and attempting to correlate any deficiencies with the stage of retinopathy. As outlined below, not all studies seem to arrive at the same answer. Some of the discrepancies occur because of differences in the methods used to analyse colour discrimination ie differences in test sensitivities. It is also possible that the differences could be attributed to some studies not making the necessary adjustments for different lens densities in the patient and control groups. The use of lens-adjusted control groups when diabetes is under investigation may be especially crucial as patients with diabetes can develop lens changes earlier than age-matched non-diabetic patients.
Investigations of colour vision in patients with diabetic retinopathy reveal a predominantly tritan defect. The FM 100 Hue total error score (TES) is higher in some patients with diabetic retinopathy than in age matched normals, (5,19-22) and both tritan (5,19,23) and diffuse defects have been reported (Figure 3). (21,23) The involvement of the S-cones is also suggested by an increased zone of foveal tritanopia (a tritanopic defect present in normal central vision due to the absence of S-cones) found in some diabetic patients. (24) A loss in the sensitivity of the S-cone pathway in patients with diabetic retinopathy has been demonstrated with psychophysical (5) and electrophysiological techniques. (25,26) Colour vision is also impaired in the presence of macula oedema and the level of impairment has been correlated with the level of the oedema. (19,27,28)
[FIGURE 2 OMITTED]
It has been suggested that the degree of diabetic retinopathy determines the degree of impairment of chromatic discrimination. The FM 100 Hue test TES and the degree of retinopathy have been correlated in some studies, (19,22,29) but others do not report this result. (5,20) The use of a battery of colour vision tests also showed a significant correlation. (7) A difference in the tritan thresholds has been reported in patients with sight and non-sight threatening retinopathy, (30) but in the same study no differences between subgroups of the two categories were found. A significant correlation between the loss in the S-cone pathway sensitivity and degree of retinopathy has also been found. (5)
Some researchers have been able to show the presence of impaired colour discrimination before signs of diabetic retinopathy can be detected. The FM 100 Hue TES has been reported to be higher in people with diabetes with no retinopathy than in 'normals'. (22) Studies of Moreland matches report that the extent is greater in some patients with diabetes with no signs of retinopathy than in normals and is correlated with the duration of the disease. (12,31) However, a study in which the sensitivity of the S-cone pathway was measured did not report a loss in sensitivity in patients with diabetes who did not show signs of diabetic retinopathy. (5) A study that evaluated tritan contrast thresholds also found no difference between patients with non-sight threatening retinopathy and lens-equated normals. (30) Electrophysiological investigations of S-cone sensitivity also differ in their reports on whether changes can be observed in patients with no diabetic retinopathy. (25,26) It has been suggested that the tritan defects found in patients without retinopathy may be the result of not correcting the results for the altered lens density. (28)
Colour vision disturbances in glaucoma have been reported since the late 19th Century. (32) A review of colour vision deficiencies in primary open angle glaucoma (POAG) estimated that 20-40% of patients have normal colour discrimination, 30-50% have tritan like defects, 5% show red-green defects, and 20-30% have a general loss of chromatic discrimination. (32)
The changes in colour vision associated with glaucoma are separate from those that occur as a result of the natural ageing process of the eye. For example, a study in which age- and lens-density control groups were used showed that the FM 100 Hue error scores were higher in patients with glaucoma than in the control group. (33)
Chromatic discrimination can also be affected in eyes with ocular hypertension. The measurement of discrimination thresholds revealed impairments in both chromatic mechanisms of colour vision (34-36) (Figure 4) and the impairment has been significantly correlated with the length of time of diagnosis of ocular hypertension. (35) However, an investigation of chromatic discrimination by a different group of researchers in a small group of patients with ocular hypertension did not find that this is any different from normals. (32)
Longitudinal studies of colour vision in ocular hypertension have evaluated whether impairment in discrimination can be used to predict the likelihood of an eye with ocular hypertension developing glaucoma. Studies have shown that the FM 100 Hue test TES obtained by patients with ocular hypertension is worse in those eyes that subsequently go on to develop glaucoma than those that do not. (35,37) The TES in those patients who developed glaucoma gradually worsened with time. (35) Abnormal tritan matches on the anomaloscope have also been linked to an increased risk of progression from ocular hypertension to glaucoma. (37) However, there was a considerable group of patients who developed glaucoma but did not show an abnormal TES or tritan match.
The correlation of colour discrimination with other parameters usually evaluated in glaucoma or glaucoma-suspect patients has also been investigated. Correlations of the FM 100 Hue TES with the severity of the field defect (38) and visual field indices (mean deviation (MD) and corrected pattern standard deviation (CSPD)) have been reported. (35) Correlations of discrimination along the protan and deutan axes with visual field parameters as well as with the cup to disc (CD) ratio of the optic disc have also been described. (36) However, these findings are not consistent. For example, in a study that corrected the FM 100 Hue TES for age, no correlation of visual field and colour defects was reported for most age groups with glaucoma and none was found in the glaucoma-suspects. (39) Some investigations of chromatic discrimination in normal tension and high-tension glaucoma report that the effects are more significant in individuals with high IOP than those with a normal IOP. (40,41) However, once again, this is not a consistent finding in all research. (42)
[FIGURE 3 OMITTED]
The studies described above probe colour vision function at the fovea. Chromatic discrimination in extrafoveal regions is also impaired in some patients with glaucoma. (43,44) Some eyes with ocular hypertension show a similar impairment of colour discrimination at eccentric locations, (43,45) but this has not been confirmed by all researchers. (32) A study of peripheral colour discrimination in patients with ocular hypertension over a five-year period did not reveal a significant correlation between chromatic discrimination and an individual developing glaucoma. (46) At the follow up, the only difference between the ocular hypertensive group and glaucomatous group was along the protan axis. This led the researchers to conclude that an increase over time in colour discrimination thresholds along the protan axis may be an indicator of an eye with ocular hypertension developing glaucoma.
[FIGURE 4 OMITTED]
There is a history of using short-wavelength (blue) stimuli on a yellow background to examine the visual field of patients with glaucoma or those who are suspected of having the disease. The bright yellow background is used to adapt the long-wavelength sensitive cones (L-cones) and medium-wavelength sensitive cones (M-cones) and to saturate the rods; the short-wavelength target (blue lights) is used to maximise the response of the S-cone system. It has been shown that visual field defects in glaucoma suspects can be detected earlier by this method of short wavelength automated perimetry (SWAP) than with standard white-on-white perimetry. (47,48) Indeed, visual field defects in patients with glaucoma are sometimes more extensive with SWAP. (48) The short-comings of SWAP, however, include longer testing times and increased variability. (49)
Although most reports on colour defects in glaucoma concentrate on ocular hypertension and POAG, an evaluation of colour perception in individuals with angle closure glaucoma revealed significantly higher scores on the FM 100 Hue test compared to those without this disease, (50) with 40% of eyes having a Type 3 tritan-like defect. Experimentally-induced elevation of IOP also results in a reversible Type 3 tritan defect. (51)
In summary, it is well-established that colour discrimination is impaired in glaucoma, especially along, but not confined to, the tritan axis. Whether early detection of an impairment in hypertensive eyes can be used to identify eyes that will go on to develop glaucoma remains a matter for further research, but it is likely that computerised measurements of chromatic discrimination thresholds rather than clinical tests will need to be used.
Investigations of colour discrimination in patients with age-related maculopathy (ARM) reveal a tritan defect, but the ability of clinical tests to detect this depends on the severity of ARM. For example, an examination of patients with ARM showed that 6 out of 11 subjects failed the D15 test, (52) with most showing a tritan defect. However, no definitive defects could be found in the majority of patients who were classified as pre-ARM (VA of 6/7.5 with retinal changes). (52) Studies in which the desaturated D15 test was used also showed that the results were worse in patients with ARM than in age-matched normals. (53,54) An examination of patients with retinal pigmentary changes but normal VA also revealed impaired colour vision when the desaturated D15 test was used. (54) However, in a different study, the desaturated D15 proved too variable to differentiate between those with and those without ARM22 The results of the FM 100 Hue test were also shown to be normal in early ARM. (55)
The measurement of tritan discrimination thresholds with a computerised method revealed higher thresholds in patients with ARM that varied with the severity of the disease. (56) An examination of the S-cone pathway also showed reduced sensitivity for patients with ARM compared to normals. (57) Additionally, patients with soft drusen had lower sensitivity than those with hard drusen.
Central serous retinopathy
Central serous retinopathy (CSR) is characterised by symptoms of reduced vision and metamorphopsia. A Type 3 tritan colour vision defect with a pseudoprotanomalys (58) has also been reported in CSR. An improvement of colour discrimination is observed as the disease resolves. However, in a number of patients a tritan-like colour defect may persist even when the VA has returned to normal. (59)
Optic neuritis is an inflammatory disease of the optic nerve. In some patients, the disease is associated with multiple sclerosis. A sign of optic neuritis may be the desaturation of colours in the affected eye. A study of 438 patients with optic neuritis reported that in the acute phase of the disease, only 6.8% of patients were classified as having normal colour vision using the FM 100 Hue test, 54% were classified as having abnormal colour vision, with the rest not being able to perform the test. (60) Optic neuritis has sometimes been associated with a predominantly red-green colour defect, (61,62) but discrimination along the tritan axis is often also affected, to the same or even greater degree. (60,63-66) Furthermore, in some patients the type of colour defect may change over time. (60,64) The colour vision defect may even remain after recovery of VA. (60, 67)
Dominant Optic Atrophy
Dominant optic atrophy (DOA) is a hereditary disease. Examination using a battery of colour vision tests, including the evaluation of colour discrimination ellipses, indicated that no individual patient with DOA had an isolated tritan defect, (15) although in most the impairment of tritan discrimination was greater than that of red-green discrimination. Differences in the nature of the defect were observed within the same families. It has been speculated that this variation may be a reflection of genotypic variations.
A problem anywhere along the visual pathway can give rise to an acquired colour vision defect. Colour vision defects have therefore also been reported in patients with cerebral lesions. (68,69) Although tritan defects are common, (7) red-green discrimination can also be affected. Colour vision defects have been found in patients with normal VA and no symptoms of impaired vision. (68) In some patients, a complete loss of colour vision (achromatopsia) can occur as a result of a cerebral lesion. (67,70)
Medication side effects
Disturbances of colour vision have been reported as a side effect of a number of medications as well as with exposure to certain chemicals. The information about colour vision disturbances can be particularly useful if it can be used as an early sign of toxicity.
Digoxin and Digitoxin
Digoxin and Digitoxin are used in the treatment of heart arrhythmias and heart failure. Toxicity has been associated with a predominantly red-green colour deficiency. (71,72) The correlation of the FM 100 Hue TES with levels of the drug in blood serum suggested that an elevated score could be used as a sign of toxicity. (73,74) However, the number of errors found in plate tests and the D15 was not correlated with serum levels of the drug. (75) A study in which a battery of colour vision tests was used concluded that colour vision disturbances cannot be used to diagnose toxicity, as disturbances along both colour axes were also common in patients who did not show signs of digoxin toxicity and were receiving therapeutic levels of the drug. (75)
Sildenafil Citrate (Viagra)
In its course of action, Viagra has an inhibitory effect on an enzyme (PDE6) found in the retina. (76) The effects of Viagra on visual function have therefore been investigated. The use of Viagra has been linked with an impairment of colour discrimination in the blue/green region (tritan-like). This appears to occur at the same time as the plasma levels of the drug peak. The defect is transient and dose-related. (76)
Chloroquine is used to treat rheumatoid arthritis, systemic lupus erythematosus (SLE), and malaria, as well as being used as a malaria prophylactic. The drug can accumulate in the retina and lead to chloroquine retinopathy. Tritan discrimination is affected first but in more advanced cases discrimination along the protan axis is also impaired. (77) In a study that used a battery of clinical tests to evaluate colour vision in patients with chloroquine retinopathy, the majority failed at least one colour vision test but the sensitivities of the tests varied. (78) An evaluation of colour discrimination ellipses indicated that the loss is either along the tritan axis or is diffuse, and is related to the accumulated dose. (79)
Ethambutol is used in the treatment of tuberculosis. Toxicity can lead to an optic neuropathy in which a predominantly red-green defect becomes apparent, but disturbances of tritan discrimination have also been reported. (80-82) The visual function does not always recover when the drug is withdrawn. (83)
Investigations of medications used in the treatment of epilepsy showed that some give rise to an impairment of triton discrimination. (84,85) When colour discrimination defects were found, these were significantly correlated with other signs of neurotoxicity. (84)
Disturbance to colour vision has also been reported as a result of exposure to industrial chemicals, eg solvents. (86) In general, when colour vision is affected, the deficiency is tritan in nature and dose dependant. For example, this is true in the exposure to styrene used in factories producing reinforced plastics. Studies that investigated exposure to solvent mixtures, eg in the painting or printing industry, have yielded various results. (86) When a colour defect was reported, it again affected tritan discrimination. Exposure to elemental mercury vapour can also result in a tritan defect that is dose dependant. (86) A reduction in the levels of exposure to mercury reversed the defect.
The assessment of acquired colour vision defects in the optometric practice presents itself with a number of challenges. Acquired defects do not follow the well-defined characteristics of congenital deficiencies and may be difficult to classify. A battery of tests will often be needed to detect the defect and to determine its severity. Although some researchers have used clinical colour vision tests, most recent studies use specifically designed, computerised tests to evaluate colour discrimination in acquired deficiencies. Those methods may also be needed to detect the small differences in chromatic discrimination that could, in some instances, be used to predict the progression of a disease or to signal toxicity.
Module questions Course code: C-12174
Please note, there is only one correct answer. Enter online or by the form provided
An answer return form is included in this issue. It should be completed and returned to CET initiatives (c-12174) OT, Ten Alps, 1 New Oxford Street, High Holborn, London, WC1A 1NU by December 18 2009
1. Which of the following about progressive red-green blindness, as described by Kollner, is TRUE?
a. The blue-yellow system is nut affected
b. The blue-yellow system is affected but less than the red-green system
c. The defect is most likely to be caused by a disease of the retina
d. The defect does not occur in conjunction with blue-yellow blindness
2. According to Verriest's classification, a Type 1 red-green defect is characterised by:
a. Protan-like discrimination and a normal spectral luminosity function
b. Deutan-like discrimination and a normal spectral luminosity function
c. Deutan-like discrimination and a spectral luminosity function in which the wavelength of maximum sensitivity is shifted towards shorter wavelengths
d. Prutan-like discrimination and a spectral luminosity function in which the wavelength of maximum sensitivity is shifted towards shorter wavelengths
3. Acquired colour vision defects:
a. Are more common in males than females
b. Do not regress even if the disease process regresses
c. Become apparent only in the advanced stages of ocular or systemic disease
d. Can be seen in the early stages of ocular or systemic disease
4. Which of the following tests is the MOST suitable for assessing an acquired colour vision deficiency?
a. Rayleigh match
b. Hardy Rand Rittler plates
c. Ishihara Test
d. City University Test
5. Which of the following about the Farnsworth Munsell 100 Hue test is TRUE?
a. The axis of colour confusion can always be easily identified
b. The result is not affected by the patient's age
c. The results are affected by the patient's age and other factors
d, The results are affected by the patient's age but not by any other factors
6. Age-related changes of the crystalline lens:
a. Are solely responsible for the increase in the FM 100 Hue error score with age
b. Affect colour discrimination but do nut affect colour matching
c. Give rise to a predominantly red-green colour vision defect
d. Give rise to a predominantly tritan colour vision defect
7. Which of the following points to an impairment of the S-cone system in diabetes?
a. A larger area of foveal tritanopia
b. A smaller area of foveal tritanopia
c. A smaller area of foveal protanopia
d. An increase in the sensitivity of the S-cone pathway
8. Most patients with primary upon angle glaucoma show:
a. Normal colour discrimination
b. An impairment of chromatic discrimination along the tritan axis
c. An impairment of chromatic discrimination along the red-green axis
d. A general loss of colour discrimination
9. Which of the following about colour vision in Age-Related Maculopathy is TRUE?
a. Assessment of colour vision is usually nut possible due to reduced VA
b, A predominantly red-green defect is usually found
c. A predominantly tritan defect is usually found
d. The sensitivity of the L-cone pathway is usually affected
10. Which of the fullowing about colour vision defects in optic neuritis is TRUE?
a. They regress completely as soon as VA returns to normal
b. They may remain even when VA returns to normal
c. They rarely occur during the acute attack of the disease
d. They are static during the progression of the disease
11. Dominant optic atrophy gives rise to:
a. Tritan defects only
b. Red-green defects only
c. Red-green or tritan defects
d. Achrematopsia only
12. Which of the following has been reported in advanced cases of chloroquine retinopathy?
a. Normal colour discrimination
b. Type 1 red-green defect
c. Type 2 red-green defect
d. Type 3 tritan defect
Monika Formankiewicz is a senior lecturer in the Department of Optometry and Ophthalmic Dispensing at Anglia Ruskin University. Her PhD work concentrated on colour and spatial vision. Monika is a member of the Anglia Vision Research group.
Monika Formankiewicz BOptom MCOptom PhD
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|Title Annotation:||COLOUR VISION PART 3: COURSE CODE: C-12174|
|Article Type:||Disease/Disorder overview|
|Date:||Nov 6, 2009|
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