Note from archiver<at>cs.uu.nl:
This page is part of a big collection
of Usenet postings, archived here for your convenience.
For matters concerning the content of this page,
please contact its author(s); use the
source, if all else fails.
For matters concerning the archive as a whole, please refer to the
or contact the archiver.
Subject: sci.med.vision: Frequently Asked Questions (FAQ), Part 3/5
This article was archived around: 19 Feb 1997 08:31:55 +1100
Version: $Id: faq-part3.txt,v 1.15 1996/03/13 00:40:28 grants Exp grants $
FREQUENTLY ASKED QUESTION: Vision and EyeCare
(Copyright(C), Grant Sayer)
+ Section 4: Disease of the Eye (Anterior Eye Disease) +
This section, and the subsequent section, are only an overview of some
of the typical problems and questions that have appeared in the sci.med news
groups. It is not a complete discussion of all the potential ocular diseases,
which of course, would occupy a complete medical textbook. At this stage
it has been broadly classified into anterior and posterior, for want of
a better classification scheme.
Also note that the information on eye disease is only provided as an
information service and does not replace examination by an eyecare
Some attempt has been made to include references to World Wide Web pages
which may have more information and/or graphics on the disease.
Conjunctivitis is an inflammation of a mucous membrane and therefore in most
types there is a red eye, thickening of the conjunctival tissue and some
discharge of mucous or mucous and inflammatory cells. The causes
of Conjunctivitis include; bacterial infection, viral infection and allergic
Typical bacterial conjunctivitis, is caused by the common staphylococcus and
diplococcus pneumoniae to the less common organisms of the haemophilus group.
Infection is generally in both eyes with the patient experiencing
discomfort in the form of a "smarting" and grittiness, moderate photophobia,
but minimal pain. Discharge from the infection causes the well known symptoms
of eyelids stuck together on wakening or having a "crusty" appearance.
Bacterial conductivities responds well to antibiotic treatment.
Viral infections, sometimes caused by adenoviruses which are often involved
in upper respiratory tract infections, cause inflammation of the membrane
on the back of the eyelid.
Allergic conjunctivitis results from hypersensitivity to exogenous antigens.
There are many forms, with some examples being, profuse watering due to hay
fever, chronic inflammation as a result of a reaction to locally applied drugs.
The treatment is to remove the antigen and use of vasoconstrictors
4.3 Dry Eyes
- Causes [Details to be added ]
- Treatments, in-eye solutions, tear duct plugs [details to be added ]
( pharmaceutical company that manufacturers dry eye products. Also
includes pictures of dry eye)
(Sjogrens Sydnrome Foundation)
(Dry Eye Institute)
4.4 Eyelid Problems
Styes are common eyelid problems and are a type of "boil" involving an eyelash
follicle. There is generally a tense swelling with redness and pain, until the
abscess escapes. Application of local heat, using a compress can assist in
easing the pain and bring the stye more quickly to a "head".
Internal stye, tarsal cyst or chalazion is a chronic granuloma of the
Meibomain gland of the eyelid. This manifests as a small hard spherical
lump within the eyelid, often easily felt but not seen. Treatment varies,
depending on the size and/or associated discomfort which may be caused by
the swelling of the eyelid.
Other common eyelid problems include blepharatis, which is a kind of
"dandruff" of the eyelid margin. The eyelid margins are red-rimmed with
flakes and scales among the eyelashes. Burning discomfort and itching
comes and goes. Treatment involves cleansing of the eyelid margin,
using sterile wipes or eye ointments.
Keratoconus (conical cornea) is an recessive inherited condition usually
apparent between the ages of 10-25yrs. Incidence of the condition is
approximately 1 in 5,000.
The condition manifests as a thinning of the corneal apex, or central area
of the cornea. With the weakening of the tissue there is a bulging of the
tissue which increases the myopia of the affected eye. Initial correction
is via spectacles whereby reasonable vision can be attained. Subsequent
treatment is via a rigid contact lens which will provide a new front
surface to the optical system of the eye.
There is more information about this condition from the CLEK study at
Other sources of information for readers in the USA are
National Keratoconus Foundation (310) 855-6435
National Eye Institute (301) 496-5248
NORD (National Organization for Rare Disorders) 1-800-799-6673
US Public Health Service 1-800-336-4797
4.6 Herpes Zoster ("Shingles")
Affects the eye by encroaching from a skin lesion or starts on
the eye. The appearance is white pustules, similar to cold sores
in the mouth. This disease is treated by early antiviral
4.7 Effects of Radiation on the Eye
4.7.1 General Effects of Radiation on the eye
UV radiation is classified as
Potential hazards from UV radiation are photokeratitis, conjunctivitis
and lenticular cataracts (Elliot et.al - see reference below).
Parrish JA, Anderson RR, Urbach F, Pitts D. "UV-A Biological effects of
ultraviolet radiation with emphasis on human responses to longwave
ultraviolet", New York, Plenum, 1978
- UV radiation less than 320nm causes photokeratitis
- large doses of wavelengths greater than 350nm are required to
induce cataract formation, perhaps of the order of
0.5 to 1.0 MJ/m^2
4.7.2 Visual Displays and Radiation
From the Journal of Theoretical Biology 1986, 122, 491-492 as a letter
to the editor from Liden, Bergqvist and Wennersten they comment that
the CRT worker has less exposure to UV-A than other office workers. The
details of the radiation levels are given below
UV-A Detector's Direction UV-A (W/m^2, mean)
Towards the screen at 60cm distance 0.03
Towards the ceiling (VDT operators) 0.04
Towards the ceiling (other office workers) 0.13
The author's conclusions were that UV-A emmission from VDT's is very low
and can not be of biological relevance in comparison to normal UV-A exposure.
Also that VDT work and health is a multi-factorial problem and that a
common single-factor explaination of ill health during VDT use is not viable
In another paper -
Elliot G., Gies P., Joyner K.H, and Roy C.R. "Electromagnetic radiation
emmissions from video display terminals (VDTS)", Clinical and Experimental
Optometry 69.2: MArch 1986, pp53-61.
- report that there is no ocular hazard from the RF emmissions from VDTs.
Also that VDTs emit no UV radiation below 350nm.
This is postulated as a means of determining general health by variations
in the iris pigment and structure
Some papers and references (contributed by Roberty Sekuler from
Sekuler R. and Blake R., "Instructors Manual to accompany Perception",
McGraw-Hill, Third Edition, 1994, pp4-5) which tested and debunked
A Simon, DM Worthen and JA Mitas, An evaluation of iridology, Journal of
the American Medican Association, 1979, 242, 1385-1389.
P Knipschild, Looking for gall bladder disease in the patient's iris.
British Medical Journal 1988, 297, 1578-1581. In this paper five
iridologists were asked to judge stereo color slides of the right eyes
of various people for signs of gall bladder disease. According to
iridology texts, gall bladder is projected in the lower lateral part
of the right eye's iris. Further, gall stones are supposed to induce
small, dark spots in that part of the right iris, while inflammation
of the gall bladder is said to induce white line there. Among the slides
that were to be judged for telltale signs of gall bladder disease
were slides of the right eyes of patients who were to have their gall
bladders removed the next day. The slide set also contained slides of
the right eye of age- and gender-matched controls, presumably free of
gall bladder disease. Now the results: the five trained iridologists did
really well in spotting gall bladder disease in the eyes of patients who
actually had g.b. disease. They judged 56% of the patients' slides
as showing evidence of gall bladder disease. Unfortunately, they gave
just about the same percentage of FALSE positive --identifying people
as having g.b. disease who actually did not. Too bad that the experiment
included those pesky control measurements!!!
But those interested in pursuing it further there are locations of
Iridologists on the WWW -
+ Section 5: Disease of the Eye (Posterior Eye Disease) +
5.1 Floaters and Spots in the Field of View
Floaters (muscae volitantes - "flying flies") are spots before the eyes of
different shapes, sizes and number. They appear often when looking at a
plain coloured field of view, eg blue sky, a wall. Typically when the patient
tries to look at them they report that the spots "run- away". The spots are
due to corpuscles circulating in the retinal vessels and specks within the
vitreous. These opacities cause shadows to be cast onto the retinal
sensory apparatus; the rods and cones; and thereby appear as dark spots in
the field of vision. Slight cases or observations require no treatment.
There are other retinal and vitreous conditions that may cause increased
presence of floaters indicative of more serious complications, for example,
vitreous or retinal detachment. It is therefore advisable in the presence
of an increased occurrence of floaters that you get a check-up by a
5.2 Macular Degeneration
The macular is the innermost part of the central retina; an area where the
retina has the highest concentration of cones (sensory apparatus of vision).
The degeneration which occurs within this area of the retina can be due to
a breakdown of the retinal receptor cells, leakage of exudate between the
retinal layers and occasionally destructive bleeding.
As a result of the changes to the retina there is a decrease in central vision,
often with little to no involvement in the peripheral retina. Hand magnifiers,
spectacle magnifiers and low vision aids can be used by the patient to assist
More information can be obtained from the National Eye Institute located
in Bethesda, MD on (301)496-4000.
Internet Resources include:
(contains 2 pages including photographs of macular degeneration conditions)
(information on preventing macular degeneration with dietary carotenoids
a medical sciences bulletin)
( medical research and development with information on Ophthalmic research)
5.3 Retinal Detachments
The retina is one of the three layers of the human eye. The innermost layer
is a complex and delicate layer (0.4mm in thickness) which lines the innerside
of 2/3rds of eyeball. There are a number of sub-layers to this tissue which
comprise the neural layers and photoreceptors necessary for vision.
Detachment of the retina is a separation of the neural retina from the pigment
epithelium; a layer of pigment cells providing nutrients to the photreceptors
and attaching the retina to the next outermost layer - the choroid. As a
result of the separation there is a loss of function in the photoreceptors,
vision is affected.
The accompanying symptoms of a retinal detachment include; blurring of vision,
sensation of "flashing lights", loss of vision like a shade or curtain moving
across the field of vision. The presence of a retinal detachment is a serious
visual problem and should be thoroughly investigated by an eyecare professional.
Retinal detachment occurs in some hereditary conditions, e.g Stickler
Syndrome. More information is available on the Web at
(contains fundus photograph)
5.4 Diabetes and The Retina
Diabetes causes a number of retinal changes which can include haemorrhages,
micro-anueryisms of the capillaries, exudates, abnormalities of arteries
and veins and retinal detachment. The combination of these changes can result
in reduced vision to severe complications. The examination of the status of
the diabetes and it's impact on the retina is assessed with a technique called
Other information is available at
(contains detailed information on diabetes and particular section on
diabetic eye disease which includes questions and answers)
5.5 Retinitis Pigmentosa
Retinitis Pigmentosa is a degeneration of the retinal pigment epithelium.
This is a single celled layer of pigment cells that is between the retina
and the choroid, the second "coat" of the eye. In this condition pigment
granules are lost from the epithelium layer and deposited in clumps in the
See section [11.1] for details of a listserv group that discusses the
This listserv (RPLIST@sjuvm.stjohns.edu) contains the following information
GET RPLIST VITAMIN -> two letters regarding E. Berson's vitamin A study
GET RPLIST TRANSPL -> an article on retinal cell transplants
GET RPLIST REFSUM -> an article on Refsum's disease
Internet Resources include:
(contains 2 pages including photographs of macular degeneration conditions)
Glaucoma is a symptomatic condition and not a disease "sui generis". It
is a collection of physicals signs: raised intra-ocular pressure, visual
field loss, enlargement of the blind spot and changes in the appearance of
the optic nerve head. There are a variety of clinical classifications of
- eyedrops to reduce aqueous fluid production, increase fluid drainage.
- laser trabeculotomy to increase outflow of the aqueous humor.
Glaucoma may be defined as "those situations were IOP is too high for
normal functioning of the optic nerve head (Shields, 1992.) IOP is closely
linked to aqeous humor (clear, watery, fluid in the eye) dynamics. IOP is a
function of aqeous humor outflow (AHO) and production (AHP) (IOP = AHO -
AHP). Therefore pharmaocological treatment is aimed at either increasing
outflow or decreasing production of aqeous humor. IOP is measured by many
different types of machines by your health care proffesionals. These exams
are important because as with hypertension, when symptoms are noticed by
the patient the damage has already been done.
For patients who are refractory to medical treatment a surgical operation
is performed. This operation makes an external drainage system for the AH
and thus increased outflow. This proceedure called a trabeculectomy, is
done in the operating room with local anesthesia. Sucess rates for normal
risk patients is very high.
OTher information located on the Web includes:
(information on the condition including cross section of the eye and
optic nerve head fundus photography)
(extensinve information on glaucoma including FAQ's on the disease, medication
research and drug information)
(maintains a listserver for ophthalmic specialists, and FAQ's - under
(manufacturer of visual field equipment which is used for testing of
effects of glaucoma.)
Cataracts are opacifications of the crystalline lens of the eye, causing a
loss of transparency. The crystalline lens is the "focussing" mechanism
of the human eye. The change in light transmission is due to accumulation
of water and/or denaturation of the lens protein. A variety of factors
cause cataracts, eg diabetes, eye trauma, age related changes. The
predominant symptoms of cataract are an increasing loss in vision. There
can be associated fluctuations in the vision depending on water changes in
the lens. The rate at which the cataract changes varies depending on
The surgical procedure is described below (contribued by Dr W.Wan M.D):
There are two standard techniques for modern cataract surgery:
phacoemulsification (PE) and nucleus expression or planned extracapsular
cataract extraction (ECCE). There are numerous variants on these,
especially PE, which may get advertised as no-stitch, one-stitch, clear
cornea, topical, etc. In general: 1) PE is technically more difficult to
learn, however, once you learn it, most surgeons feel it is a better
technique in their hands; 2) the incidence of complications is dependent
on the surgeon and the patient population, not the particular technique
used (PE was previously thought to have a greater incidence of
complications, but this was primarly due to a learning curve; for a given
surgeon, the complication rate will be lowest with the technique that he
is best with); and 3) PE is generally quicker than ECCE, but again this is
My personal preference is for PE 95% of the time; ECCE is reserved for
cases where it may be better than PE based on the type of cataract, the
patient, the surgical goals, and occasionally the type of equipment
available. (If you want to know how I decide which are in that 5%, you
need to go to ophthalmology residency!) PE generally offers quicker visual
recovery, and arguably quicker healing and overall rehabilitation, better
wound stability, and less risk of disastrous complications such as an
expulsive hemorrhage during surgery. However, the bottom line is, good
surgeons get good results with either technique, pick a surgeon who gets
good results and let him decide what technique is best for you in his
hands. (Even then, of course, keep in mind that although it is 95%
successful, cataract surgery IS surgery, and complications can occur.)
The indication for removing the cataract in a second eye is the same as
the first: If the decreased vision in that eye is bothering the patient.
(Unless there is some other eye disease, e.g. glaucoma or inflammation
being caused by the cataract, or it is preventing management and treatment
of some other eye problem in the interior of the eye, which would be
unlikely if it is mild.)
Other internet resources that provide information on cataracts
(Eye Radiation and Environmental Research Laboratory)
(EyeCare Connection homepage with information on cataracts)
(Lens and Cataract Researcher Internet Directory)
( American Society of Cataract & Refractive Surgery - patient FAQ on cataract)
[ TBD - details to be added ]
(The Wilmer Eye Institute - has a page on ocular immunology )
(The Virtual Medical Centre)
(SUNY at Buffalo Ophthalmology Dept - Case presentation on ocular
pathology and uveitis)
5.9 Ocular Migraines:
AAN migraine information
[ The following information was contributed by D.Nelson M.D
(firstname.lastname@example.org - ]
The following is an attempt to give an_introduction_only to this vast
subject with protean manifestations.
Migraine affects about 10% of the population. It affects all ages from
babies to adults although age does seem to have a protective quality.
The general mechanism seems to be a constriction of blood vessel(s) followed
by a dilation the the vessel. The aura (when present) accompanies the
vasoconstriction and the headache (when present), the vasodilation.
There are identifiable "trigger factors" notably:
1. certain foods. Caffiene (coffee, colas, chocolate), citrus fruits,
alcohol, nitritate and nitrites, aged cheese, and others.
2. hormonal changes esp. puberty, pregnancy, menopause and "the pill".
3. fatigue/stress. This can be physical (heat/cold) or emotional
4. bright lights
5. loud noises
7. refractive error
As well, there are cerain associations with migraine. Cyclic vomiting as a
child, car or motion sickness, a family history of migraine, drusen of the
5.9.2 Classification of migraine:
I. Common migraine. The comprises about 80% of those with migraines. It is
the typical "sick headache" possibly with mood changes. The headache can
be localized or generalized. It may last for hours to days.
II.Classical migraine. The triad of aura, headache, nausea+/-vomiting, and
a feeling of "being out of sorts". It is typically of shorter duration
than the common migraine. The aura may be any sort of neurologic
deficit but of course the ones we see are usaully visual. The visual
aura usually starts near fixation and expands to the periphery then
dissappears to be followed by the headache. The aura may be jagged,
coloured lines, "grey blotches" or "missing patches" or many other type
of visual disturbance. Classical migraine account for about 10% of migraines.
III. Complicated migaine (expanded below)
3.Retinal (or ocular, see below)
IV. Cluster headaches SEVERE episodic unilateral head or facial pain,
nasal stuffiness, +/-ipsilateral Horners, lacrimation.
Complicated migraine expanded:
This is a headache which may be severe and focal neurologic signs which last
longer than the headache. This is the hallmark of the complicated migraine
in which the neurologic deficit may even be permanent. For example, there
can be permanent visual field defects.
2. Ophthalmoplegic migraine
The patient is usually young (less than 30, usually less than 20). There is
a severe unilateral headache. As_the_headache_clears, one or more ocular
muscles on the side of the headache become paretic and may take days or
weeks to recover their function. As you can appreciate, the first time this
happens, the patient is subjected to a lot of investigations including
angiograms as this is mimicing such things as aneurysm, tumour and other
very bad things. If the ophthalmoplegia recurs, the sequence of events and
the previously negative tests are reassuring.
3. Retinal migraine (ocular migraine)
The patient is typically under 40 and suddenly loses a portion (retinal) or
all (ocular) of the visual field in one eye. There is rarely headache.
Never, according to some experts. The differentiation between retinal and
ocular migraine is how much of the visual field is affected. In other
words, what vessel has been affected. If it is distal to the bifurcation at
the optic nerve head, it is retinal. If it involves the central retinal
artery, all of the vision is lost and it can be called ocular migraine. Note
too, that there are seldom if ever flashing lights with this form of
migrain. Again, the vision recovers (ususally, sometimes permanent) in 20
to 45 minutes. With ocular migraine there can be retinal hemorrhages,
vitreous hemorrhages. macular edema, ischemic swelling of the optic nerve.
4. Basilar migraine
Mimics vertebrobasilar attacks. Bilateral blurred vision, vertigo, ataxia,
nausea, incoordination, loss of balance, speech difficulties.
There is a host of symptom-complexes which fit the criteria for migraine.
Sudden, episodic, self-limited, lasting 30-45 minutes. These can be chest
pains, vomiting, neurologic symptoms and many others. These are sometimes
called migraine equivalents.
The most common migraine type problem that I see in my practice is that of a
person who may or may not have previously had migraine diagnosed who has a
15-30 minute episode of visual disturbance, often quite classically starting
off small near fixation and expanding to fill a hemifield. When the
probable diagnosis is explained to the patient, the response is almost
invariably "Oh, but it can't be migraine, I don't have a headache!"
Remember, if it walks like a duck and quacks like a duck, it's probably
Choroiditis is an inflammation of the choroid, the second "coat" of the
eye. This tissue layer is a vascular rich layer located between the
sclera (outer white coat) and the retina (sensory layer).
+ Section 6: Binocular Vision Problems +
6.1 Strabismus (Turned Eye)
A squint or strabismus is a failure of the two eyes to look at the same
object thereby preventing binocular vision. Human binocular vision develops
during the first few years of life. Interruption to the motor, sensory or
central components, for example nerve or muscle defect, can lead to sensory
or central defect. Causes of many squints are not fully understood although
the majority are either a hereditary factor or a responsible defect.
Such factors causing squints include;
+ ocular abnormalities that prevent good central vision,
eg congenital cataract.
+ paresis of one of the eye's muscle
+ brain damage, eg cerebral palsy
+ large refractive errors, eg accommodative esotropia
Refractive errors are an important causative factor to strabismus since it
can prevent clear vision - impeding development of the sensory mechanism,
and affecting the normal relationship between accommodation and convergence.
When the eye's require vision at a near distance there both a movement of the
two eyes (convergence) and change in focus (accommodation).
A child that is hypermetropic (long sighted) has to accommodate more than is
normally required for distance and near vision. Because of the linkage
between accommodation and convergence the excess accommodation causes an
excess convergence of the two eyes. The result, in a young child whose
visual system is still developing is what is called a convergent squint.
When binocular vision is disturbed double vision results. Young infants are
able to suppress one of the images to one eye to remove the double vision
that occurs at the onset of strabismus. The effect of the suppression of
the image causes the vision in the "squinting" eye to fail to develop
normally. This is called AMBLYOPIA. There are other visual abnormalities
that can develop as a result of squint.
The treatment for squint depends on the cause. Some essential treatments
+ search for ocular defects
+ refraction and glasses to remove any refractive errors
+ patching or occlusion of the eyes to prevent amblyopia
+ surgical adjustments to the muscles of the eye.
These treatments aim to remove amblyopia, restore binocular vision and if
necessary cosmetic corrections to the appearance of the turned eye.
6.2 Amblyopia ("Lazy Eye")
Amblyopia is defined by Schapero et al. as the condition of reduced visual
acuity which cannot be corrected by refractive means and is not attributed
to structural or pathological ocular anomalies.
Acuities of worse than 20/30 (6/9) are considered to meet the criteria of
amblyopia according to Griffins reference on Binocular Anomalies.
There are a variety of classifications of amblyopia, in general the categories
are organic or functional. Examples of organic amblyopia include;
+ nutritional, e.g poor diet in the case of alcoholism
+ toxic, e.g methyl alcohol poisoning or salicylate poisoning
+ congenital, e.g bilateral or unilateral central scotoma at birth.
Functional amblyopia also has three classifications;
+ hysterical, e.g psychogenic causes giving central visual field defect
+ refractive, e.g uncorrected isometropia resulting in poor visual
+ strabismic, e.g long standing suppression in cases of strabismus
Commonly used therapy for amblyopia is occlusion or lens therapy in the
case of refractive. The patching is associated with general to increasing
eye-hand coordinated tasks to stimulate development of the amblyopic eye.
6.3 Problem(s) When Wearing Glasses
- Misaligned centres affecting binocular vision.
[ TBD ]
6.4 Vision Therapy
Common problems that require vision therapy include
+ accommodation insufficiency
+ accommodation excess
+ convergence insufficiency
+ convergence excess
Treatment is often by a combination of either lenses or prisms with
or without convergence training.
The next level of 'therapy' is the tracking exercises, eye-hand coordination
and similar coordination tasks.
Details of the training is beyond the scope of this FAQ and the
interested reader/patient is recommended to seek professional
6.4.2 Bates Method
Vision therapy, especially people claiming improvement of vision through
'holistic' medicine can often lead into a *very* heated debate. The
techniques generally describe some form of eye excerise associated with
relaxation technique to improve the 'perception' of letters/images. There
is limited to virtually no statistical studies/results indicating the
success or failure of these methods.
Often the central theme is to "to getting the eyes to shift more rapidly,
to get you centre of focus to hit directly on the fovea, and to
reduce tension in the eyes so that the above can be accomplished".
As described by one internet reader (email@example.com) the
method for improved sight involves :
1) KEEP YOUR EYES MOVING. Your eyes have to be fast to catch all the
2) GET LOTS OF SUNLIGHT. Don't be afraid of the sun. If it's too bright
3) WEAR A PATCH. If you do this even for as little as fifteen minutes,
4) STRETCH YOUR NECK. If your neck is cramped, then so are your eyes.
Some references are
Bates, William Horatio. The Bates method forbetter eyesight without
glasses. New York : Holt, Rinehart, and Winston, 1981, c1943.
Corbett, Margaret Darst. Help yourself to better sight. New York,
Corbett, Margaret Darst. A quick guide to better vision; how to have good
eyesight without glasses, 1957.
Huxley, Aldous. The art of seeing. Seattle : Montana Books, 1975.
Goodrich, Janet. Natural vision improvement. Berkeley, Calif. Celestial
Kaplan, Robert-Michael. Seeing beyond 20/20. Hillsboro, OR: Beyond Words
Seiderman, Arthur. 20/20 is not enough : the new world of vision. New
York : Knopf : Distributed by Random House, 1989.
Kavner, Richard S. Total Vision. New York : A & W Publishers, 1978.
Windolph, Michael. Easy eye exercises for better vision : self-helps to
sight improvement. Hicksville, N.Y. : Exposition Press, 1974.
Chaney, Earlyne. The eyes have it : a self-help manual for better
vision. New York : Instant Improvement, 1991.
Revien, Leon. Sportsvision : Dr. Revien's eye exercises Program for
athletes. New York : Workman Pub., 1981.
Scholl, Lisette. Visionetics : the holistic way to better eyesight.
Garden City, N.Y. : Double day, 1978.
Hughes, Barbara. 12 weeks to better vision : a remarkable technique to
restore your eyesight. New York : Pinnacle Books, c1981.
+ Section 7: Colour Vision Problems +
7.1 Defective Colour Vision:
Defects in colour vision, often incorrectly referred to as colour
"blindness" fall into two main categories:
(a) Congenital Colour Vision Defects
(b) Acquired Colour Vision Defects
The distinction between the two varieties are that acquired defects are
often the result of some disease process which affects the colour vision
receptors or higher neural pathways. Congenital colour vision defects
are genetically related.
7.2 Classification of Congenital Colour Vision Defects
Colour vision defects are classified via the number of primary spectral
colours which an individual requires to match any other spectral colour.
The normal individual usually requires 3 primaries and is classified as
(a) Achromatic (Monochromatic) Colour Vision
+ no colour vision
+ only light - dark discrimination
+ lack of retinal function (typical case)
+ higher centre defects (generally atypical)
(b) Dichromatic Colour Vision
+ colour distinctions of 2 kinds (achromatic or R-G/Y-B)
+ 4 types
- protanopia and deutranopia (confusion of colours from green
through yellow to red)
- tritanopia and tetartanopia (confusion of colours from blue
through green to yellow.
(c) Trichromatic Colour Vision
+ anomalous type requires 3 stimulus primaries to match stimuli
but matches are outside the normal range
+ 3 types - protan, deutran, tritan
The colour defective person has difficult in distinguising colours that
are on "confusion lines". For example, protanopes confuse blue-greens
(and greys) with red (and browns). The deutranopes make mistakes with
blue-greens and purple. While tritanopes confuse yellow with violet.
The last dichromat group; tetartanopes, confuse yellow with blue. The
anomalous types have difficulty with light tints and dark shades.
Colour defective vision is inherited as a sex-linked recessive characteristic.
It is more common in men than women. The most common defect is
deutranomoly with an incidence of 5% or males, protanomaly affects 1.5% and
protanopia and deutranopia about 1% each.
7.3 Classification of Acquired Colour Vision Defects
Acquired colour vision problems can be the result of lesions of the macula,
optic nerve, or visual cortex. Also changes in the optical media, eg cataract
changes, or toxic effects of chemicals can alter colour perception.
Acquired colour vision defects are generally asymmetrical in the two eyes,
eg affecting red-green as well as yellow-blue, while also there may be
other defects of visual function ( visual field defects).
7.4 WWW Resources on Colour
Information on Gamma and Colour are contained in Charles A Poynton's FAQs
EMAIL: firstname.lastname@example.org PHONE: +61-2-805-2937
SNAIL: Canon Information Systems Research Australia
1 Thomas Holt Drive, North Ryde, Australia 2113