Vision of Children: Information for Families

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Frequently Asked Questions About Ocular Albinism

What is Ocular Albinism (OA)?
What causes OA?
How many genetic variations of OA have been identified?
How common is OA?
What are the features of OA?
How soon after birth can these features be detected in an infant?
Will the nystagmus lessen with age?
How does OA affect the development of the eye from conception onward?
What is the general range of acuity measured in individuals with OA?
Why can't OA be corrected by wearing corrective eyeglasses or contact lens?
Is there any examination that can reliably prognosticate visual acuity for infants with OA?
Is OA a progressive or degenerative condition?
Are there other physical conditions that commonly occur in conjunction with OA?
Is OA commonly misdiagnosed? If so, why?
What is the difference between ocular albinism (OA) and oculocutaneous albinism (OCA)?
Do some kids with OCA have normal hair and skin pigment?
Is there a DNA test available for OCA? Where can I find out about it?
Do people with OA always have fair skin, blonde hair and blue eyes?
Do people with OA need to be careful about sun exposure to their skin and eyes?
Are there any particular ethnic groups or geographic areas of the world where OA is more common?
How is OA inherited? Please explain the genetic inheritance pattern.
What is the percentage chance of OA carrier mothers passing the OA gene to their sons? Daughters?
Do females ever have OA? How does this occur genetically?
Will males with OA pass the OA gene to their sons? Daughters?
What are the long-term indications for individuals with OA? Are they able to lead independent lives, participate in sports, drive a car, attend 'regular' school?
What programs are available in public schools to help kids with OA?
Why are so many patients given incorrect, overly negative information about their potential abilities to function with OA?
Are there any developmental problems associated with OA?
Is there a diagnostic test available to test for OA for either carriers or people who may have it?
How may I obtain information about having this test performed?
Is there any research being conducted to find a treatment or cure for OA?
Does the government fund any research on OA?
Is there any treatment or surgery currently available for OA? Nystagmus?
As a parent/guardian, what is the most important thing I can do to help my OA child function successfully in the world?
Where can I find other people/families affected by OA?
Are there any conferences I can attend to learn more about OA?
How can I help in the quest to find a cure for OA?

1) What is Ocular Albinism (OA)?
Human albinism can be divided broadly into two types, 'Oculocutaneous Albinism (OCA)' and 'Ocular Albinism (OA)'. These terms were devised in the late 1940s, when medical science was less sophisticated than it is now. The terminology sounds simple, but in reality is probably incorrect, since all forms of albinism have relative deficiencies of pigment in the hair, skin, and eyes.

Historically, 'Ocular Albinism' is an inherited disorder in which the eyes are deficient in the amount of melanin and pigment, while the skin and hair 'appear' normal or near normal in coloration.

2) What causes OA?
Ocular Albinism (OA) results from the inability of the normal pigment cells in the eyes (especially the iris and the retinal pigment epithelium) to produce normal amounts of pigment. Exactly how the reduced amount of pigment leads to reduced visual acuity, nystagmus, and sensitivity to sunlight is not yet clear, nor is it necessarily true that the pigment itself is primarily responsible, but rather some other developmental pathway in the assembly line of the eye and of visual development.

3) How many genetic variations of OA have been identified?
In most cases, Ocular Albinism is X-linked. That means that the gene for it is located on the X-chromosome. Historically, X-linked Ocular Albinism is also called Nettleship-Falls Ocular Albinism, after the two physicians who defined its characteristic occurrence among males and the visible features in the retina among females who are carriers for the condition.

Some years ago a series of families were described in which children of normally pigmented parents had the ocular features of albinism but did not appear to have significant cutaneous hypopigmentation. This was called autosomal recessive ocular albinism (AROA) because males and females were affected in these families. Studies now show that calling this AROA is not correct and most of the individuals and families like this have OCA1B or OCA2 with nearly normal or normal cutaneous pigmentation. One family has been described in which the individual with OCA1B was not diagnosed with albinism until mid-life, although she had always been aware of her reduced visual acuity.

4) How common is OA?
The population frequency of Ocular Albinism is unknown. Healthcare statistics in North America do not tabulate the frequency of these disorders. Educated estimates vary between 1 person in 20,000 to 1 person in 50,000. It is likely that the incidence of Nettleship-Falls albinism is more prevalent than 1 person in 50,000 due to frequent misdiagnosis.

5) What are the features of OA?
The features of Ocular Albinism include: reduced visual acuity (typically from approximately 20/30 to approximately 20/400); nystagmus (an uncontrollable, pendular, rapid movement of the eyes back and forth); strabismus (a muscle imbalance of the eyes in which the eyes are 'crossed' rather than straight and parallel); and sensitivity to bright light. The reduced visual acuity may result in difficulty at school, such as trouble reading what is on a blackboard, except when the reading material is held very close, and difficulty with sports, particularly with small projectile objects. The reduced visual acuity may ultimately limit an affected individual's ability to obtain a driver's license, because most states require at least 20/70 vision (best corrected with glasses or contact lenses) to obtain at least a daylight-restricted driver's license.

6) How soon after birth can these features be detected in an infant?
That depends, especially on the care with which the parents look for subtle changes in the newborn infants. Oftentimes, the nystagmus is not present at birth but develops between three weeks and eight weeks after birth. The sensitivity to sunlight may not be appreciated for many months, and the reduced visual acuity many not be detected until an infant is cooperative enough to understand the task of recognizing figures, numbers, and other objects. However, in a family with Nettleship-Falls Ocular Albinism in which there are other known affected males and the mother is known to be a carrier, examination of a male infant at or shortly after birth should clarify whether any individual male is or is not affected.

7) Will the nystagmus lessen with age?
Generally, the nystagmus does dampen or reduce in time, especially after age 5-8 years. Nystagmus never completely disappears, even in adults, although most adults with nystagmus are able to control it to a significant extent.

8) How does OA affect the development of the eye from conception onward?
Two major problems with the eye and ocular development include abnormalities in the development of the central vision area of the retina (called the 'macula' or the 'fovea') and in the conduct of impulses from the retina through the optic nerve to the brain.

The most obvious feature inside the eyes of individuals with Ocular Albinism is underdevelopment of the fovea, the small area in the center of the retina that provides fine central vision (reading, recognizing faces). In OA, the fovea does not develop completely, presumably because the amount of melanin and pigment needed for growth processes that normally occur after birth is not present. As a result, and perhaps for other reasons, the eye cannot process sharply focused light images. Because this sensitive nerve tissue in the retina does not develop normally, visual acuity cannot be corrected to normal even with glasses or contact lenses, because the 'film in the camera' is incapable of taking a complete picture and transmitting it to the brain normally.

The second alteration is the transmission of images through the optic nerve. The nerve pathways through the optic nerve to the brain do not follow the usual pattern of routing. In the normal eye, nerve fibers from each eye go to both sides of the brain, that is, the same side as the eye and the opposite side of the eye. In eyes with Ocular Albinism, more of the nerve fibers cross from one eye to the opposite side of the brain. These same eye problems occur in individuals with oculocutaneous albinism (where the albinism more dramatically affects the skin and the hair as well as the eye).

9) What is the general range of acuity measured in individuals with OA?
Reduced visual acuity less than 20/20 is essentially always present. However, visual acuity best corrected in young adults and adults with Ocular Albinism may be as good as 20/30 or as bad as 20/400 and anywhere in between.

10) Why can't Ocular Albinism be corrected by wearing corrective glasses or contact lenses?
Two features affect the final visual outcome. Underdevelopment of the center vision of the retina (the 'fovea') does not allow the 'film of the retina' to take an accurate picture and thus transmit an accurate picture to the brain. Second, because both the transmission of images and the balance of wiring from each eye to each side of the brain are altered, the brain cannot interpret the impulses correctly and the image is less than perfect. Thus, even when the image is accurately focused with the proper glasses prescription or contact lens prescription, the film in the back of the camera does not take a good picture and the computer does not receive a good transmission.

11) Is there any examination that can reliably prognosticate visual acuity for infants with Ocular Albinism?
A test called a Visually Evoked Potential (VEP), or sometimes called a Visually Evoked Cortical Potential (VECP), is performed like an EEG or brain wave test. This test will show, when each eye is stimulated independently, the differences of transmission from the stimulated eye to each side of the brain. However, in infants, since the visual pathways continue to develop until at least 7-9 years of age, nothing in an infant will predict exactly what the final visual acuity will be.

12) Is OA a progressive or degenerative condition?
In general, as children with Ocular Albinism mature, their visual acuity seems to improve. Part of this 'improvement' may be progressive maturation of the nerve pathways in the brain. Some of this, of course, is maturation of the infant or child to understand the task of visual acuity, reading letters and recognizing figures on a screen. However, there is no evidence that OA is degenerative, and most adolescents and young adults maintain that vision throughout life. Individuals with OA never go totally blind from this disorder, although they may be legally blind.

13) Are there other physical conditions that commonly occur in conjunction with OA?
Males with X-linked Ocular Albinism tend to have lighter skin and lighter hair than their unaffected brothers and sisters. Some of them will also have blotchy skin changes with relative hyper- and hypo- pigmentation. However, no other systemic constitutional disease is associated with X-linked OA. Parents of children with OA need to be watchful for development of strabismus (when the eyes do not fixate and track together). Uncorrected strabismus leads to amblyopia, which can further impair vision severely.

14) Is OA commonly misdiagnosed? If so, why?
There are several pitfalls in the diagnosis of OA, just as there are for oculocutaneous albinism (OCA) in general. The first is the frequent misdirection of the infant who presents with nystagmus (the pendular or rhythmic uncontrollable movement of the eyes). Children with this finding are sometimes referred to neurologists for evaluation of brain tumors or other developmental aberrations of the brain, and are not referred to ophthalmologists. Both should be consulted until a definite diagnosis is reached. Sometimes, well-intended but unsuspecting ophthalmologists fail to look at the whole child and compare the color of the skin and hair to other siblings (if there are any) at comparable ages. Third, infants and children of European-American ancestry tend to be 'blonde' anyway and may escape notice if other siblings are not available for comparison. Lastly, the ophthalmologist may fail to look carefully at the iris for transillumination, or they mistake the absence of normal retinal development for 'foveal hypoplasia' or other neurologic problems. Even if the diagnosis of 'albinism' is made, the ophthalmologist may frequently fail to examine the mother, and most importantly, to dilate the mother's pupil to look for the classical features of the carrier state of X-linked OA described in 1951 by Dr. Harold Falls.

15) What is the difference between ocular albinism (OA) and oculocutaneous albinism (OCA)?
Sometimes, very little other than the gene which causes them. The vision problems experienced by those with OA and OCA are virtually the same. The hair color and skin pigment can vary significantly between OA and OCA, even though those with either condition typically have reduced pigment compared to unaffected siblings.

16) Do some kids with OCA have normal hair and skin pigment?
Yes, some people with OCA (primarily OCA1B) have nearly normal hair and skin pigment just like people with OA.

17) Is there a DNA test available for OCA? Where can I find out about it?
Testing for OCA1 and OCA2 is available on a research basis in the Pigment Laboratory at the University of Minnesota. The tyrosinase gene is responsible for OCA1. Sequence analysis identifies 50-80% of the causative mutations depending on the phenotype (OCA1 vs OCA1B). The P gene is responsible for OCA2. The sensitivity of the sequence analysis is currently unknown. The P gene analysis is complex because the gene has many missense non-pathologic polymorphisms, and because there is no readily available assay of the gene product. No prenatal diagnosis is available. Information can be obtained by calling 612-624-0144 or visiting the website at www.cbc.umn.edu/iac.

18) Do people with OA always have fair skin, blonde hair and blue eyes?
No, because racial and ethnic characteristics play a considerable role in the development of the 'normal' pigmentation. Certainly, among European-Americans, many infants have fair skin and light hair. However, males with X-linked OA may have quite brown or even almost black hair and eyes of various colors ranging to light brown. However, most males with X-linked OA do have fair skin when compared to their unaffected siblings at comparable ages, and almost all of them will burn their skin in the sun before they tan. In African-Americans and Hispanics, the skin changes can be quite subtle, particularly among 'light-skinned' African-Americans. Some males will have blotchiness or patches of skin that are quite fair. Hair color is typically lighter than unaffected siblings and parents, however.

19) Do people with OA need to be careful about sun exposure to their skin and eyes?
Yes, all people with any form of albinism should use sun-protective clothing, hats, and lotions with high SPF (sun-protective formula) numbers (>15) on their exposed skin. Advice should be sought from a dermatologist.

20) Are there any particular ethnic groups or geographic areas of the world where OA is more common?
Ocular Albinism has been described throughout the populated continents of the world.

21) How is OA inherited? Please explain the genetic inheritance pattern.
The gene for OA1, Nettleship-Falls Ocular Albinism, is located on the X-chromosome, on the so-called short arm. Its pattern of inheritance is called 'X-linked'. This means that the gene is incorporated into the X-chromosome. A male has two sex- determining chromosomes, one called an X-chromosome and one called a Y-chromosome. The Y-chromosome determines 'maleness'. Therefore, if a male inherits his only X-chromosome with the X-linked OA gene on it, he must necessarily be affected with this condition. Females, however, have two X-chromosomes, one of which is inherited from their mother and one of which is inherited from their father. Females are therefore 'carriers' if they have one X-chromosome with a normal gene on it and the other X-chromosome with the X-linked OA gene on it. (They bear it within themselves, or 'carry' it.) However, in about 80 to 90 percent of females, a partial effect from the one copy of the X-linked OA gene occurs. Some females will have patches or islands of skin that are lighter pigmented than others and do not tan to the same degree. This is especially noticeable among Hispanic and African-American carriers. More impressively, females who are carriers show a mosaic (like bathroom tile) alternating patches of under pigmentation and excessive pigmentation inside the eye, becoming dramatically coarser as one leaves the central retina and extends out toward the retinal periphery. However, most females who are carriers have no visual deficit related to this condition, have normal visual acuity (perhaps with glasses), and do not have nystagmus.

In any one pregnancy, a woman who is a carrier for X-linked Ocular Albinism may transmit to her fetus either her normal X-chromosome or her OA X-chromosome with equal probability. Every child may inherit either one or the other, but not both and not either. If she transmits her normal X-chromosome, and her husband transmits his (normal) X-chromosome, the child will be XX, a girl, and both Xs will be normal, and the girl will be normal. If the mother transmits her normal X and the father transmits his Y-chromosome, the child will be XY, a boy, and a normal boy. If the mother transmits her X-linked OA X-chromosome and her husband transmits his (normal) X, the child will be XX, therefore, a girl, but will have one copy of the OA gene, and therefore, be a carrier just like her mother. Lastly, if the mother transmits her X-chromosome with the OA gene and her husband transmits his (normal) –chromosome, the child will be XY, but the only X-containing information is the abnormal gene, and therefore the child will be a male affected with OA.

22) What is the percentage chance of OA carrier mothers passing the OA gene to their sons? Daughters?
As we have just discussed, a female carrier for X-linked Ocular Albinism has four possible outcomes to any one pregnancy, each with equal probability: a normal female, a carrier female, a normal male, or an affected male. Thus, with any one pregnancy, there is one chance out of four to have an affected male and one chance out of four to have a carrier female. However, looking at the same information differently, every single daughter has one chance in two to be a carrier, and every single son has one chance in two to be affected.

23) Do females ever have OA? How does this occur genetically?
As in several other uncommon X-linked disorders, where females appear to be affected, this may result from two genetic mechanisms. The first is an abnormal structure of the X-chromosome or abnormal constitution of chromosomes. For example, we have seen several females with Ocular Albinism of the X-linked type who have a medical condition called Turner Syndrome, in which the apparent females do not have 46 chromosomes as in normal females, but rather 45 chromosomes, including only one X and no second sex-determining chromosome. Thus, from the genetic perspective, they look like females but behave like males because their only sex-determining chromosome has the X-linked OA gene on it (and there is no Y-chromosome). In some other unusual situations, there is 'skewing' in the activation or the activity of the X-chromosomes, in which the majority of cells in the developing fetus contain the X-linked OA gene active, whereas the normal gene on the other X-chromosome becomes inactive. Therefore, the majority of tissues appear to have the OA gene in effect. Also, females could inherit OA if their father is affected and their mother is a carrier.

24) Will males with OA pass the OA gene to their sons? Daughters?
An affected father has his X-linked Ocular Albinism gene on his only X-chromosome and he has a normal Y-chromosome. Every time he transmits his Y-chromosome, he will have a male since the Y-chromosome is normal. All the sons of the affected male are normal (unless by some unusual possibility he happens to marry another carrier female). If, however, he transmits his only X-chromosome with the X-linked OA gene on it, and his wife contributes only her normal X-chromosomes, every single daughter of this male will be a carrier.

25) What are the long-term indications for individuals with OA? Are they able to lead independent lives, participate in sports, drive a car, attend 'regular' school?
For the majority of males with the Nettleship-Falls type of Ocular Albinism, the long-term implications are quite good. They certainly are able to live independent lives, to participate in educational and sporting activities, and to attend 'regular' schools. Sometimes, special adaptations, low vision aids, high magnification chip cameras and close circuit TVs, and other visual enhancements may be necessary. The ability to drive an automobile requires good visual acuity (in addition to good judgment). In most states, driver's licenses can be obtained by those individuals whose best-corrected visual acuity is at least 20/70 in at least one eye. A substantial fraction of individuals with the Nettleship-Falls X-linked Ocular Albinism have visual acuity in that range.

26) What programs are available in public schools to help kids with OA?
There are three federal laws in the United States which may have some application and benefit to education of children with albinism, one of which applies solely to education. They are IDEA (Individuals with Disabilities Education Act); Section 504 (public accommodation for handicapped person); ADA (Americans with Disabilities Act).

IDEA has two components, EIS (Early Intervention Services) for children birth to three years of age or kindergarten, and regular IDEA coverage for school-age children. Under both programs there are a number of set classifications which automatically entitle children to special assistance through an individualized plan, called an IFSP for EIS children, and an IEP for school-age children. The individualized plan is determined through evaluation of the child by the local IDEA administrator which may be the school district or another state or quasi-public agency, depending on the way the state has set up its IDEA program, each state having certain leeway to design and implement the program as it sees fit.

In addition to the administrative evaluation, the administrative agency must have a meeting at least once a year with the parents about the plan. Parents may invite anyone they wish to attend the meeting and advocate certain services to go into the plan. This could be an independent evaluator such as a pediatric ophthalmologist, low vision optometrist, developmental pediatrician, and/or an attorney, or any other people the parents want to attend. Parents must sign off on the plan. If they don't and the administrator will not satisfy the parents' concerns and requests, a hearing process is followed, and the local decision can be reviewed at the state and federal level on proper request.

Sufficiently low vision, amounting to legal blindness, should automatically qualify children for IDEA coverage. Where children do not have sufficiently low vision to qualify, another 'delay' or area of difficulty may have to be identified by evaluation of the administrator independently. Even where a school-age child does not qualify for IDEA, they may be entitled to a Section 504 plan if the parents request an evaluation for same.

Types of services and reasonable accommodations available through the public schools and other agencies which can be included in an individual plan are requirements that:

A vision therapist visit an EIS child at home or in a center on some periodic basis (one hour/week for example)
A physical therapist work with an EIS child periodically
An occupational or speech therapist monitor an EIS child periodically
Therapeutic riding, gymnastics or other recreational therapy be provided to an EIS child
A child be allowed to sit in front of the class or leave his seat to go to the front to read or copy information
A child not have to share books
A child wear a hat, sunglasses or sunscreen when outdoors
A child be allowed to wear a hat indoors
A child receive teachers' notes rather than having to copy off the blackboard
A black or white board be used instead of a green board
Shades be drawn to reduce glare
Classroom lighting be filtered or artificial glare otherwise reduced
A child be provided large print books
A child be provided large print handouts
All handouts be printed in 14-point type
The teacher not use script
The child be provided a tilt board, a laptop computer, extra time for testing, and even an aide trained in low vision teaching as often as reasonably necessary

One frequently included accommodation ion IDEA and Section 504 plans for children with nystagmus is that they take standardized testing by circling the answer in the answer book rather than filling in the dots on the computerized answer sheet (the teacher goes back and fills in the dots for them based on the answer book marks) since children with nystagmus often have trouble with keeping lines straight and staying on course through the answer sheets.

The foregoing list is not exhaustive. Parents often have to be the educators in low vision accommodation, as may schools do not have personnel experienced, knowledgeable, or trained in this field. If needed, the school must hire such individuals, or contract for their services, to accommodate children. It may be advisable to meet with the special service coordinator for the school district a year in advance of a child entering school to provide sufficient notice for the school to make any personnel changes and any budgetary changes needed to reasonably accommodate the child.

Some individual plan accommodations can undoubtedly be obtained without formal evaluation and classification with a good, sensitive teacher who cares, listens, learns, observes, and follows through with parental requests and his or her own initiative. People with Ocular Albinism successfully completed school before IDEA and Section 504 were enacted. However, one teacher who is not inclined to go the extra mile without an administrative mandate may cause an otherwise unwarranted delay in academic development.

27) Why are so many patients given incorrect, overly negative information about their potential abilities to function with OA?
X-linked Ocular Albinism, as well as other forms of Albinism, are uncommon conditions. In our highly specialized world, even pediatric ophthalmologists who deal with problems of vision in infants and children frequently may not see more than an occasional person with this over a 20 year career. Similarly, children move, are lost to continuing care, or grow up and move on to adult ophthalmologists or optometrists for their continuing ocular care. As a result, many physicians and optometrists tend to be 'negative' or at least uninformed about the potentials of visual function and development in Ocular Albinism.

28) Are there any developmental problems associated with OA?
In the usual setting, the answer is 'No'. However, one or two very rare events have been documented, in which a chromosomal deletion (a loss of a piece of the chromosome including the X-linked Ocular Albinism gene and a number of other genes in the same area) occurs, rather than a 'misprint' within the OA gene itself. Children with this deletion may have deafness, developmental retardation, and mildly shortened stature compared to their unaffected siblings.

29) Is there a diagnostic test available to test for Ocular Albinism for either carriers or people who may have it?
About 85%-95% of carriers for X-linked OA can be detected by an ophthalmologist after dilation of the pupil and careful examination of the internal contents of the eye with an indirect ophthalmoscope and other binocular instruments. The characteristic feature of the mosaic pigmentation, especially knowing the examination of the affected male child, will secure the diagnosis. Diagnosis at a DNA level, using blood samples, is available at the Baylor College of Medicine, Houston, Texas and the Laboratorio Biologia Molecolare Clinica in Milan, Italy.

30) How may I obtain information about having this test performed?
Contact information is available on this website.

31) Is there any research being conducted to find a treatment or cure for Ocular Albinism?
Yes, The Vision of Children Foundation has been supporting and funding research to find a treatment or cure since 1993. Current information concerning the solution can be found elsewhere on this website.

32) Does the government fund any research on Ocular Albinism?
In 2000, the Committee on Appropriations in the US House of Representatives urged the National Eye Institute to support research on Ocular Albinism diagnosis and treatment. In January 2002, the National Eye Institute issued a national request for proposals for Ocular Albinism research and announced it will award up to $3 million in grants to as many as seven research institutions this year for its first ever research in to the disease.

33) Is there any treatment or surgery currently available for OA? Nystagmus?
The evaluation and care of any child with X-linked Ocular Albinism includes a complete medical eye examination, not only initially to secure the diagnosis, but also to look for visual complications, particularly any unusual degrees of farsightedness, unusual degrees of nearsightedness, or exceptional astigmatism. Any of these would place the child in spectacle correction (and adolescents and young adults possibly in contact lenses). Since the fundamental defect in this condition involves the development of the retina and the central visual area before birth, and because the misrouting of the optic nerve fibers to the brain occurs long before the child is born, there is no surgery to 'correct' Ocular Albinism.

Various investigational procedures have been done to operate on the muscles outside the eye to dampen the nystagmus. However, although this surgery may have some apparent improvements, there is no clear comparison group in which a study has randomly assigned individuals to surgery and to no surgery to determine whether there is benefit from the surgery compared to the natural history of the disease, in which the nystagmus tends to dampen over time anyway.

34) As a parent/guardian, what is the most important thing I can do to help my OA child function successfully in the world?
The single most important thing that any parent can provide for his child is education. The second most important step, especially in children with visual impairments, is never to accept a self-fulfilling prophecy. (An example of a self-fulfilling prophecy is a statement by a physician: 'Well, your child will never ride a bicycle'. As a result, you never buy the child a bike. Guess what? The child never learns to ride a bicycle.)

35) Where can I find other people/families affected by Ocular Albinism?
You may sign up on this website to become a member of our family e-mail network.

36) Are there any conferences I can attend to learn more about OA?
The Vision of Children Foundation is planning the 6th World Symposium on Ocular Albinism, which will be held in Fall 2006 in San Diego, California. The National Association of Albinism and Hypopigmentation also sponsors conferences for people affected by albinism. Information is also available from the American Nystagmus Network.

37) How can I help in the quest to find a cure for OA?
By supporting The Vision of Children with your donations. Over 80% of the funds raised go directly to support research. Also, if you are willing to write letters or contact your Congressman to encourage federal funding of research, please contact VOC for coordination of these efforts.

The Vision of Children would like to thank Dr. Richard Lewis, Professor, Departments of Ophthalmology, Medicine, Pediatrics, and Molecular and Human Genetics, Cullen Eye Institute, Baylor College of Medicine, and Vicky Vaught, Director, NOAH and ANN, for their invaluable contribution in formulating and answering these important and common questions about Ocular Albinism.

The Vision of Children Foundation
12671 High Bluff Drive, Suite 300 | San Diego, CA 92130
Phone: (858) 799-0810 | Fax: (858) 794-2348 | E: jleonard@visionofchildren.org