|
Colour blindness is the inability to distinguish certain colours.
It occurs when one or more of the cone types is missing or defective
to any extent. They may be absent entirely, or may be present, but
unable to manufacture the necessary signals to the brain. It is
characterized by abnormal colour matching and colour confusions.
Colours which look different to people with normal colour vision
can look the same to people with defective colour vision. For example,
grass may appear green to colour normals, but be the same colour
as orange for people with certain colour defective vision. There
is also a marked reduction in the number of separate colours that
can be distinguished in the spectrum and the relative luminous efficiency
of the eye is altered.
Types of Colour Vision Defects
Trichromatic Possess all three cone pigments and has normal colour
vision.
Dichromatic - Has complete deficiency in one cone pigment
but preserves the remaining two cone pigments.
Monochromatic - Has only one cone pigment.
Achromatopic Possesses no functioning cones.
Dichromats have two cone receptors rather than three, and
match all the spectral hues using two colour matching variables.
There are three types of dichromatism depending on which of the
three normal pigments is missing. Protanopes are the most common,
lacking the long-wave red sensitive receptors. Deuteranopes
lack the middle-wave green receptors, and tritanopes
lack the short-wave blue sensitive receptors. Protanopes
and deuteranopes cannot distinguish red light from green light,
while the rare tritanope has blue-yellow confusion2.
Anomalous Trichromatic is the name given to partial deficiencies
in one of the three cone pigments. This means that to match a reference
colour, three test colours must still be used, but the match is
different from normal. e.g. a protanomalous trichromat requires
more red than normal to match the reference2.
Protanomaly is deficiency in sensitivity to red, as well
as poor red-green discrimination. A deficiency of green sensitivity,
as well as blue-green and yellow-green insensitivity is called deuteranomaly.
Tritanomaly is the deficiency of the cone pigment for blue as well
as blue-green and yellow-green insensitivity2.
Monochromacy occurs when two of the types of cones malfunction
resulting in single cone vision. This is relatively rare, with an
incidence of about 1 in 30,000. Characteristics include reduced
visual acuity, usually around 6/60 (20/200) but occasionally significantly
better, scotopic spectral sensitivity with no Purkinje shift (shift
from vision with rods, to vision with cones), photophobia (sensitivity
to light), nystagmus ("wobbly eyes", where eyes are constantly
trembles, and does not fix on a target normally) which usually disappears
by age 30 years, and sluggish pupil reflex to light1.
Achromatopsia is the complete absence of any cones, or a
very low normal cone density. The achromat can only see in black,
white and shades of grey. Typical complete achromatopsia is characterized
by reduced visual acuity from infancy, photophobia, pendular nystagmus
that may diminish during adolescence, absence of foveal reflex,
and irregular distribution of macular pigment1.
Defects arising during life can be due to general or ocular disease,
a side-effect of medication, or as a consequence of toxic poisoning
or head trauma. Changes in colour vision can be one of the first
indications of disease, and are generally progressive. It is important
to identify the cause early to avoid permanent damage1.
Most acquired colour vision defects come on gradually or suddenly
and are easily identifiable, since they usually involve other abnormal
visual symptoms such as reduced vision, a constriction of the field
of vision in general or in a specific region, poor adaptation to
the dark, etc. Acquired defects are often confined to one eye or
one part of the visual field.
A test is available online, but should not be used as a substitute
for a test carried out by your optician, if you have any concerns
with your colour vision then please visit your optician or call
the Zeidan Centre.

|