vision loss

Choroidal Dystrophy, Central Areolar 2

Clinical Characteristics
Ocular Features: 

Slowly progressive loss of vision is noted in the 4th and 6th decades with a mean age of onset at 46 years. ERG recordings suggest that the cone dysfunction is more severe and occurs earlier than rod deterioration.  Night blindness is usually not a major complaint.  A central scotoma is usually present but peripheral fields may be relatively intact.  Dyschromatopsia is often present.  Early in the disease the RPE may have a granular appearance but in later stages there is usually a sharply demarcated area of central RPE atrophy (sometimes called geographic atrophy).

Autoflourescence, pattern ERGs, and fine matrix mapping can reveal abnormalities before patients become symptomatic.

Systemic Features: 

No systemic features are known.

Genetics

This is a clinically and genetically heterozygous disorder.  Multiple mutations in the PRPH2 gene (6p21.1) have been identified in this condition.  Some of the clinical variation may be mutation-specific.

For a somewhat similar disorder see choroidal dystrophy, central areolar 1 (215500).

CACD is a genetically heterogeneous disorder with mutations in several genes responsible.  The majority of patients have one of several mutations in the PRPH2 gene (6p21.1-cen) and the inheritance pattern seems to be autosomal recessive (CACD2).  Other family trees in which mutations in PRPH2 were excluded suggest autosomal dominant inheritance (CACD3; 613144).   

The gene product of PRPH2 is important to the integrity and stability of the structures that contain light-sensitive pigments (e.g., photoreceptors). More than 100 mutations have been identified. The resultant phenotype can be highly variable, even within members of the same family but most affected individuals have some degree of pigmentary retinopathy within the macula or throughout the posterior pole.

The altered gene product resulting from mutations in PRPH2 often leads to symptoms beginning in midlife as a result of the slow degeneration of photoreceptors. This database contains at least 11 disorders in which PRPH2 mutations have been found.

Pedigree: 
Autosomal dominant
Treatment
Treatment Options: 

No effective treatment is known.

References
Article Title: 

Central areolar choroidal dystrophy

Boon CJ, Klevering BJ, Cremers FP, Zonneveld-Vrieling MN, Theelen T, Den Hollander AI, Hoyng CB. Central areolar choroidal dystrophy. Ophthalmology. 2009 Apr;116(4):771-82, 782.e1.

PubMed ID: 
19243827

Retinitis Pigmentosa 80

Clinical Characteristics
Ocular Features: 

Night blindness is an early symptom which may be noted in early childhood.  Vision loss can be documented in early childhood and progressively worsens to hand motions or light perception by the 3rd to 5th generation.  The fundus appearance has been described as normal in 1-year old patients but retinal pigmentary changes and arteriolar changes are evident in some children by the age of 2 years.  Typical bone spicule pigmentary changes have been described in some older patients.  Staring at lights (photophilia) has been noted in children under 1 year of age while eye-rubbing (oculodigital sign) may be seen soon thereafter.  Nystagmus is often present.

ERG responses are greatly diminished or nonrecordable.  Rods are more severely affected than cones.  OCT shows loss of inner and outer segments of photoreceptors.

Systemic Features: 

Systemic signs seem variable but full evaluations have not been done in all patients.  Mild developmental delay has been reported in some individuals and significant childhood onset hearing loss has been documented in at least one person.  Radiography of the hands revealed cone-shaped phalangeal epiphyses in 5 probands and one proband had short fingers in one study.

Genetics

Homozygous or compound heterozygous mutations in the IFT140 gene (16p13.3) segregates with the phenotype as expected for an autosomal recessive disorder.

The same gene is mutated in Short-Rib Thoracic Dysplasia 9 (266920) in which similar digital and retinal changes are seen.  However, renal, hepatic, and additional skeletal disease are also present.  These may be the same conditions pending further elucidation of the phenotypes.

Pedigree: 
Autosomal recessive
Treatment
Treatment Options: 

No treatment has been reported for the general disorder.  However, low vision aids should be offered to young people, especially during school years.

References
Article Title: 

Familial Exudative Vitreoretinopathy, EVR7

Clinical Characteristics
Ocular Features: 

The ocular features are primarily limited to the posterior chamber where there are areas of retinal avascularity, exudation, retinal holes, and detachments.  Areas of degeneration and pigmentary retinopathy may be present.  Vascular proliferation may be part of the process with vitreous traction and folds.  Progression of retinal damage is highly variable and surgical outcomes are unpredictable.  Long term vision outcomes are sometimes as good as 20/40 but in many eyes NLP or hand motion vision is the end result.  

Secondary changes in the anterior chamber and cornea from repeated surgeries may lead to glaucoma, cataracts, and corneal decompensation. 

Systemic Features: 

There are no consistent systemic abnormalities.

Genetics

Missense and nonsense heterozygous mutations in the CTNNB1 gene (3p22.1) segregate with this autosomal dominant condition found in two families of Japanese origin.  A Chinese 3-year-old with FEVR having a single BP insertion in the CTNNB1 gene also had global developmental delay and dysmorphic facies.

Pedigree: 
Autosomal dominant
Treatment
Treatment Options: 

The prognosis for vision is poor as the retinal damage often continues to evolve and additional folds and detachments develop.  Attempts to close retinal holes and repair detachments are important.

References
Article Title: 

Defects in the Cell Signaling Mediator β-Catenin Cause the Retinal Vascular Condition FEVR

Panagiotou ES, Sanjurjo Soriano C, Poulter JA, Lord EC, Dzulova D, Kondo H, Hiyoshi A, Chung BH, Chu YW, Lai CHY, Tafoya ME, Karjosukarso D, Collin RWJ, Topping J, Downey LM, Ali M, Inglehearn CF, Toomes C. Defects in the Cell Signaling Mediator v-Catenin Cause the Retinal Vascular Condition FEVR. Am J Hum Genet. 2017 Jun 1;100(6):960-968.

PubMed ID: 
28575650

Retinal Dystrophy with or without Macular Staphyloma

Clinical Characteristics
Ocular Features: 

Few patients have had complete eye studies and physical findings are seemingly limited to the eye.  Patients complain of progressively decreasing vision as early as the first decade of life.  Abnormal retinal findings may be present by the second decade and maybe earlier.  The RPE can appear mottled and the retinal vessels are attenuated.  Retinal pigment clumping occurs later.  Night blindness and visual field constriction occur.  Cone and flicker ERGs may be nonrecordable while rod and flash ERGs are reduced consistent with a rod-cone dystrophy.  The retinal lamination has been described as abnormal on OCT in some individuals.

Macular staphylomas have been described in three unrelated offspring of consanguineous parents.

Vision loss is severe with legal blindness by midlife and one patient lost light perception by 40 years of age.  

Systemic Features: 

No consistent systemic abnormalities have been reported.

Genetics

Homozygous or compound heterozygous mutations in the C21orf2 gene (21q22.3) are the cause of this autosomal recessive syndrome.

Homozygous or heterozygous mutations in the same gene are responsible for axial spondylometaphyseal dysplasia (602271).

Pedigree: 
Autosomal recessive
Treatment
Treatment Options: 

No treatment has been reported.

References
Article Title: 

Retinitis Pigmentosa 47

Clinical Characteristics
Ocular Features: 

Onset of night blindness and field constriction symptoms occur during the 4th and 5th decades of life.  Pigmentary abnormalities of the retina are the hallmark of this condition.  Retinal thinning, bone spicule pigmentation, vascular attenuation, optic disc pallor, and pigmentary atrophy have all been noted.

In patients with the autosomal dominant form of this disease, rod function is severely impaired or absent as evidenced by ERG studies.  Cone responses are often reduced on an age-related basis and in the range of 85-95% below normal.  As expected, dark-adapted visual thresholds are elevated and visual fields are restricted peripherally.  Loss of vision is age-related but some individuals can retain acuities of 20/35 to 20/40 into their sixth decade.  It is more common for acuities to be in the range of 20/200 to 20/400 later in life.

Systemic Features: 

No systemic disease is associated with this disorder.

Genetics

Mutations in the SAG gene (2q37) are responsible for this form of RP.  Both autosomal recessive and autosomal dominant modes of inheritance have been reported.

In one family with homozygous mutations a sib had features of Oguchi disease which also results from homozygous mutations in SAG.

Among Hispanic families in the southwestern US, heterozygous mutations in SAG are a common cause of autosomal dominant retinitis pigmentosa.

Pedigree: 
Autosomal dominant
Autosomal recessive
Treatment
Treatment Options: 

No treatment has been reported for this disorder.

References
Article Title: 

A Novel Dominant Mutation in SAG, the Arrestin-1 Gene, Is a Common Cause of Retinitis Pigmentosa in Hispanic Families in the Southwestern United States

Sullivan LS, Bowne SJ, Koboldt DC, Cadena EL, Heckenlively JR, Branham KE, Wheaton DH, Jones KD, Ruiz RS, Pennesi ME, Yang P, Davis-Boozer D, Northrup H, Gurevich VV, Chen R, Xu M, Li Y, Birch DG, Daiger SP. A Novel Dominant Mutation in SAG, the Arrestin-1 Gene, Is a Common Cause of Retinitis Pigmentosa in Hispanic Families in the Southwestern United States. Invest Ophthalmol Vis Sci. 2017 May 1;58(5):2774-2784.

PubMed ID: 
28549094

Cone-Rod Dystrophy With Decreased Male Fertility

Clinical Characteristics
Ocular Features: 

Features of a cone dystrophy appear first followed by rod damage although the course of degeneration is variable.  Poor vision may be present in some individuals in the first years of life but has a later onset in others.  Evidence for rod dysfunction appears later in most patients.

A hyperfluorescent area centered on the fovea can often be seen although there may be patchy areas elsewhere in the fundus.  Foveal atrophy is present in individuals generally after the 5th decade of life. Full field ERG shows reduced or absent cone responses with variable rod responses with more pronounced changes in older individuals.  Variable pigmentation can be seen in the peripapillary area.

Systemic Features: 

The only systemic abnormality thus far identified is a reduction in sperm count and reduced motility.  The resulting loss of fertility, however, occurs only in male patients with truncating variants in TTLL5 and not in those with missense mutations according to the most recent studies.

Genetics

This autosomal recessive condition results from homozygous or compound heterozygous mutations in the TTLL5 gene (14q24.3).  TTLL5 is localized at the base of the spermatozoal axoneme and at the basal body of the cilia in photoreceptors.  

Interestingly, male mice with mutations in this gene have reductions in sperm motility with evident disruption in the formation of sperm tails.

Pedigree: 
Autosomal recessive
Treatment
Treatment Options: 

No treatment is known.

References
Article Title: 

Mutations in the polyglutamylase gene TTLL5, expressed in photoreceptor cells and spermatozoa, are associated with cone-rod degeneration and reduced male fertility

Bedoni N, Haer-Wigman L, Vaclavik V, Tran HV, Farinelli P, Balzano S, Royer-Bertrand B, El-Asrag ME, Bonny O, Ikonomidis C, Litzistorf Y, Nikopoulos K, Yioti G, Stefaniotou M, McKibbin M, Ellingford J, Booth AP, Black G, Toomes C, Inglehearn CF, Hoyng CB, Bax N, Klaver CC, Thiadens AA, Murisier F, Schorderet DF, Ali M, Cremers FP, Andreasson S, Munier FL, Rivolta C. Mutations in the polyglutamylase gene TTLL5, expressed in photoreceptor cells and spermatozoa, are associated with cone-rod degeneration and reduced male fertility. Hum Mol Genet. 2016 Aug 22. pii: ddw282. [Epub ahead of print].

PubMed ID: 
27554115

Biallelic variants in TTLL5, encoding a tubulin glutamylase, cause retinal dystrophy

Sergouniotis PI, Chakarova C, Murphy C, Becker M, Lenassi E, Arno G, Lek M, MacArthur DG; UCL-Exomes Consortium, Bhattacharya SS, Moore AT, Holder GE, Robson AG, Wolfrum U, Webster AR, Plagnol V. Biallelic variants in TTLL5, encoding a tubulin glutamylase, cause retinal dystrophy. Am J Hum Genet. 2014 May 1;94(5):760-9.

PubMed ID: 
244791901

Retinitis Pigmentosa 72

Clinical Characteristics
Ocular Features: 

The history and fundus findings are typical for classic retinitis pigmentosa with onset of symptoms in the 4th and 5th decades or earlier. Salt and pepper pigmentation may also be present. These consist of night blindness, decreased visual acuity, and constriction of visual fields.  The fields are constricted to 10-30 degrees, and vision ranges from 20/25 to 20/40.  Optic pallor is often present, the retinal vessels are narrowed and bone-spicule pigmentation has been described.  Vitreous 'condensation' sufficient to obscure fundus details may be present.  ERG responses are absent or substantially reduced.  Heterozygotes have no symptoms or fundus abnormalities.

Systemic Features: 

No systemic features have been described.

Genetics

Homozygous mutations in the ZNF408 gene (11p11.2) are responsible for this condition.  The product of this gene is a transcription factor highly expressed in fetal and adult retina and plays a role in vasculogenesis.

Heterozygous mutations in the same gene cause familial exudative vitreoretinopathy (FEVR6) (616468) described in one family with significant vitreal and retinal vascular disease.

Pedigree: 
Autosomal recessive
Treatment
Treatment Options: 

No treatment is available for the basic disease.  Tinted lenses may provide some benefit.

References
Article Title: 

Whole-exome sequencing reveals ZNF408 as a new gene associated with autosomal recessive retinitis pigmentosa with vitreal alterations

Avila-Fernandez A, Perez-Carro R, Corton M, Lopez-Molina MI, Campello L, Garanto A, Fernandez-Sanchez L, Duijkers L, Lopez-Martinez MA, Riveiro-Alvarez R, Da Silva LR, Sanchez-Alcudia R, Martin-Garrido E, Reyes N, Garcia-Garcia F, Dopazo J, Garcia-Sandoval B, Collin RW, Cuenca N, Ayuso C. Whole-exome sequencing reveals ZNF408 as a new gene associated with autosomal recessive retinitis pigmentosa with vitreal alterations. Hum Mol Genet. 2015 Jul 15;24(14):4037-48.

PubMed ID: 
25882705

Adrenoleukodystrophy, X-Linked

Clinical Characteristics
Ocular Features: 

Virtually all patients have visual symptoms.  Loss of acuity, hemianopia, visual agnosia, optic atrophy, and strabismus are the most common features.   Neuropathy may cause a decrease in corneal sensation.  Gaze abnormalities due to ocular apraxia are sometimes seen.  Ocular symptoms often occur after the systemic abnormalities are noted.  However, there is considerable heterogeneity in age of onset and progression of symptoms.

Histopathology of ocular structures reveals characteristic inclusions in retinal neurons, optic nerve macrophages, and the loss of ganglion cells with thinning of the nerve fiber layer of the retina. 

Systemic Features: 

This is a peroxisomal disorder of very-long-chain fatty acid (VLCF) metabolism that leads to progressive neurological and adrenal dysfunction from accumulation of VLCFAs in the nervous system, adrenal glands, and testes.  The age of onset and clinical course are highly variable and there may be several forms.  The childhood form begins between the ages of 4 and 8 years but in other patients with the adult form, symptoms may not appear until the third decade of life.  A viral illness may precipitate the onset.   Symptoms of both central and peripheral neurologic disease are often present with cognitive problems, ataxia, spasticity, aphasia, and loss of fine motor control.  Hearing loss is seen in some patients.  Younger patients tend to have more behavioral problems while older individuals may develop dementia.

Adrenal insufficiency leads to skin hyperpigmentation, weakness, loss of muscle mass and eventually coma.  Impotence in males is common. 

Genetics

This is an X-linked disorder secondary to mutations in the ABCD1 gene (Xp28).  The result is a deficiency in the cellular transporter known as adrenoleukodystrophy protein that is active in perioxosomes.

Although this X-linked disorder is primarily manifest in males, between 20 and 50% of female carriers have at least some symptoms, usually with a later onset than seen in males.

There are also rare cases with an apparent autosomal recessive pattern of inheritance (NALD) (202370) having an earlier onset and more aggressive course. 

Pedigree: 
X-linked recessive, carrier mother
X-linked recessive, father affected
Treatment
Treatment Options: 

Treatment of adrenal insufficiency is important and can be lifesaving.  Low vision aids, physical therapy and special education may be helpful.  Some young patients with early disease have benefitted from bone marrow transplantation.  "Lorenzo's Oil" (a mixture of oleic acid and erucic acid) has been reported to reduce or delay symptoms in some boys.

Recent reports suggest new treatment modalities may hold promise.  Infusion of autologous CD34+ cells transduced with the Lentin-D lentiviral vector reduced major symptoms in 15 of 17 boys within 29 months after treatment.  Likewise, intrathecal baclofen treatment in two boys with rapidly advancing cerebral manifestations provided symptomatic and palliative improvement.

 

References
Article Title: 

Hematopoietic Stem-Cell Gene Therapy for Cerebral Adrenoleukodystrophy

Eichler F, Duncan C, Musolino PL, Orchard PJ, De Oliveira S, Thrasher AJ, Armant M, Dansereau C, Lund TC, Miller WP, Raymond GV, Sankar R, Shah AJ, Sevin C, Gaspar HB, Gissen P, Amartino H, Bratkovic D, Smith NJC, Paker AM, Shamir E, O'Meara T, Davidson D, Aubourg P, Williams DA. Hematopoietic Stem-Cell Gene Therapy for Cerebral Adrenoleukodystrophy. N Engl J Med. 2017 Oct 4. doi: 10.1056/NEJMoa1700554. [Epub ahead of print].

PubMed ID: 
28976817

X-linked adrenoleukodystrophy

Moser HW, Mahmood A, Raymond GV. X-linked adrenoleukodystrophy. Nat Clin Pract Neurol. 2007 Mar;3(3):140-51. Review.

PubMed ID: 
17342190

Albinism, Oculocutaneous, Type III

Clinical Characteristics
Ocular Features: 

The irides may be multicolored with the central potion light brown and the peripheral areas blue-gray.  Translucency of a punctate and radial nature is present.  Nystagmus is present in almost all cases and strabismus is present in nearly half.  Visual acuity is in the range of 20/60 to 20/200.   Photophobia is less severe than in other types of oculocutaneous albinism, possibly because the vast majority of individuals (86%) have some pigmentation in the fundus. 

Systemic Features: 

The hair in dark-skinned people may be medium brown while the skin is often light brown and subject to faint tanning.  However, the hair is often copper-red in color which has given rise to the designation rufous oculocutaneous albinism. 

Genetics

This tyrosinase-positive type of albinism is sometimes called 'rufous' (ROCA) or 'brown' (BOCA) oculocutaneous albinism and is frequently found in dark-skinned individual such as Africans, African-Americans, and Hispanics.  Like other types it is inherited in an autosomal recessive pattern.  Mutations in the tyrosinase-related protein-1, TYRP1 (9p23), are responsible which seems to lead to an arrest in melanin maturation and a decrease in the amount of insoluble melanin in melanocytes.

Other autosomal recessive types of oculocutaneous albinism are: OCA1 (203100, 606952), OCA2 (203200), and OCA4 (606574). 

Pedigree: 
Autosomal recessive
Treatment
Treatment Options: 

No treatment is available for the hypopigmentation.  However, precautions against excessive sun exposure are advised.  Low vision aids can be helpful. 

References
Article Title: 

Oculocutaneous albinism

Gronskov K, Ek J, Brondum-Nielsen K. Oculocutaneous albinism. Orphanet J Rare Dis. 2007 Nov 2;2:43. Review.

PubMed ID: 
17980020

Cone-Rod Dystrophies, AD and AR

Clinical Characteristics
Ocular Features: 

Cone-rod dystrophies (CRD) are a group of pigmentary retinopathies that have early and important changes in the macula.  Cone dysfunction occurs first and is often followed by rod photoreceptor degeneration.

Common initial symptoms are decreased visual acuity, dyschromatopsia, and photophobia which are often noted in the first decade of life.  Night blindness occurs later as the disease progresses.  A fine nystagmus is also common. Visual field defects include an initial central scotoma with patchy peripheral defects followed by larger defects in later stages.  The fundus exam can be normal initially, but is followed by pigmentary bone spicule changes, attenuation of retinal vessels, waxy pallor of the optic disc and retinal atrophy.  A ring maculopathy surrounding the fovea is usually evident.  The ERG first reveals photopic defects and later scotopic changes.  Fluorescein angiography and fundus autofluorescence generally reveal atrophic retinopathy.  Many patients eventually become legally blind as the disease progresses and some end up with no light perception.

Cone-rod dystrophies are a group of disorders separate from rod-cone dystrophies where the primary defect is in the rod photoreceptors with typical pigmentary changes in the peripheral retina. The progression of vision loss is generally slower in rod-cone dystrophies. Cone dystrophies comprise another group of disorders with exclusive cone involvement in which the macula often has a normal appearance in association with loss of central acuity.

Systemic Features: 

No systemic disease is associated with simple cone-rod dystrophies.  See below for syndromal disorders with cone-rod dystrophy. 

Genetics

Non-syndromic cone-rod dystrophies can be either autosomal dominant, autosomal recessive or X-linked and are caused by defects in at least 17 different genes.  This database entry discusses only the autosomal disorders.  See X-linked cone-rod dystrophies in a separate entry.

Cone-rod dystrophies inherited in an autosomal dominant pattern include:

CORD2 (120970) is caused by mutations in CRX at 19q13.3, a homeobox gene responsible for the development of photoreceptor cells.  These are responsible for 5-10% of autosomal dominant cone-rod dystrophy cases (602225) and can also cause one type (LCA7) of Leber congenital amaurosis (602225) and a late-onset retinitis pigmentosa phenotype.

CORD5 (600977) is caused by mutations in the PITPNM3 gene at 17p13.1. 

CORD6 (601777) is caused by a mutation in GUCY2D in a similar location on chromosome 17. 

CORD7 (603649) is caused by mutations in RIMS1 at 6q12-q13.

Mutations in AIPL1 (604392), located in the same region, usually causes a form of Leber congenital amaurosis (LCA4) as well as retinitis pigmentosa (604393) but has also been reported in a cone-rod pigmentary retinopathy.

CORD11 (610381) is caused by mutations in RAXL1 (19p13.3).

CORD12 (612657) results from mutations in the PROM1 gene (4p15.3).

Mutations in the gene GUCA1A on chromosome 6p21.1 causes CORD14 (602093).

An as yet unclassified autosomal dominant type of cone-rod dystrophy has recently been localized to 10q26.

Cone-rod dystrophies inherited in an autosomal recessive pattern include:

Mutations in ABCA4 at 1p21-p13 is responsible for 30-60% of cases of autosomal recessive CRD (CORD3; 604116) .  ABCA4 is also known to cause autosomal recessive Stargardt disease.

CORD8 (605549) has been found in a single consanguineous family and the mutation localized to 1q12-q24.

ADAM9 (602713) at 8p11 and 8p11.23 contains mutations that have been shown to cause autosomal recessive CORD9 in several consanguineous families.

Mutations in RPGRIP1 (14q11) are responsible for CORD13 (608194).

The CDHR1 gene (10q23.1) contains mutations that cause CORD15 (613660).

Other autosomal CRD disorders are CORD1 (600624) described in a single individual and possibly those due to mutations in HRG4 at 17q11.2 (604011).

Syndromal cone-rod dystrophies:

Cone-rod dystrophy may also be associated with other syndromes, such as Bardet-Biedl syndrome (209900), or spinocerebellar ataxia Type 7 (164500), autosomal recessive amelogenesis imperfecta with cone-rod dystrophy or Jalili syndrome (217080), neurofibromatosis type I (162200), and hypotrichosis with juvenile macular dystrophy and alopecia (601553).  Metabolic disorders associated with cone-rod dystrophy include Refsum disease with phytanic acid abnormality (266500) and Alport syndrome (301050). 

Cone-Rod Dystrophy 19 (615860) has been associated with male infertility as the result of mutations in TTLL5 affecting both photoreceptors and sperm.

Pedigree: 
Autosomal dominant
Autosomal recessive
Treatment
Treatment Options: 

There is no treatment for these dystrophies but red-tinted lenses provide comfort and may sometimes improve acuity to some extent.  Low vision aids can be helpful. 

References
Article Title: 

A novel locus for autosomal dominant cone-rod dystrophy maps to chromosome 10q

Kamenarova K, Cherninkova S, Romero Dur?degn M, Prescott D, Vald?(c)s S?degnchez ML, Mitev V, Kremensky I, Kaneva R, Bhattacharya SS, Tournev I, Chakarova C. A novel locus for autosomal dominant cone-rod dystrophy maps to chromosome 10q. Eur J Hum Genet. 2012 Aug 29. doi: 10.1038/ejhg.2012.158. [Epub ahead of print]

PubMed ID: 
22929024

Cone rod dystrophies

Hamel CP. Cone rod dystrophies. Orphanet J Rare Dis. 2007 Feb 1;2:7. Review.

PubMed ID: 
17270046

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