strabismus

Chorioretinopathy with Microcephaly 1

Clinical Characteristics
Ocular Features: 

The ocular features have not been well described.  Small corneas, hyperopia, pale optic nerves and a variety of pigmentary changes in the retina have been reported.  The latter may consist of diffuse, fine or granular pigmentary changes.  Areas of pigmentary atrophy are often associated with patchy areas of pigmentary clumping.  These changes are usually located posterior to the equator.  Choroidal vessels may be sparse where the RPE is absent.  It has been suggested that the patchy pattern of retinal pigmentation resembles ocular toxoplasmosis.  Strabismus is common.  One report suggests microphthalmos in a patient.  Vision has been reported as subnormal from the first year of life but no quantitative data are available.

Systemic Features: 

Microcephaly is a consistent feature.  The forehead is steeply sloped but facial size appears normal.  The palate is highly arched.  Patients often have hyperactive deep tendon reflexes and walk with a shuffling gait.  Children are often hyperactive and highly social.  Intelligence quotients are usually subnormal. No lymphedema has been reported.  At least some patients have cutis marmorata.

On MRI diffuse pachygryria is seen.  The vermis is hypoplastic and the surface area of the corpus callosum is reduced to half of normal. 

Genetics

 Parental consanguinity was present in two reported families and pedigrees are consistent with autosomal recessive inheritance with homozygous mutations of TUBGCP6 (22p22) responsible.

This presumed recessive disorder appears to be different than the autosomal dominant disorder of lymphedema, microcephaly, and chorioretinal dysplasia  (MCLMR) (152950) although molecular confirmation is lacking.

For somewhat similar disorder see Chorioretinopathy with Microcephaly 2 (616171).

Pedigree: 
Autosomal recessive
Treatment
Treatment Options: 

Treatment is supportive.

References
Article Title: 

Genetic mapping and exome sequencing identify variants associated with five novel diseases

Puffenberger EG, Jinks RN, Sougnez C, Cibulskis K, Willert RA, Achilly NP, Cassidy RP, Fiorentini CJ, Heiken KF, Lawrence JJ, Mahoney MH, Miller CJ, Nair DT, Politi KA, Worcester KN, Setton RA, Dipiazza R, Sherman EA, Eastman JT, Francklyn C, Robey-Bond S, Rider NL, Gabriel S, Morton DH, Strauss KA. Genetic mapping and exome sequencing identify variants associated with five novel diseases. PLoS One. 2012;7(1):e28936. Epub 2012 Jan 17. PubMed PMID: 22279524.

PubMed ID: 
22279524

Fibrosis of Extraocular Muscles, CFEOM1

Clinical Characteristics
Ocular Features: 

Hereditary CFEOM is a congenital, nonprogressive condition.  The eyes are usually fixed in the infraducted position about 20-30 degrees below the primary position.  Horizontal movement is absent or severely restricted.  Blepharoptosis is almost always present and patients exhibit a marked chin-up position of gaze.  Binocularity is usually absent.  Some patients have large amounts of astigmatism.  Amblyopia has been reported to occur on a refractive or strabismic basis.  However, careful examination of the optic nerve may reveal anomalies such as increased cupping, asymmetric cupping and hypoplasia and could be responsible for the reduced vision in some patients.

Neuropathologic studies in rare patients have shown defects in brainstem neural development including in one case absence of the superior division of the oculomotor nerve.  Fibrosis of extraocular muscles and Tenon's capsule as well as adhesions to the globe and between muscles have been described.   Anomalous insertions of EOMs may also occur.  An MRI can reveal atrophy of the levator palpebrae and the superior rectus muscles as well as absence or hypoplasia of the oculomotor and sometimes abducens nerves.  It is now considered that CFEOM disorders result from primary neuronal disease resulting in secondary myopathy. 

Systemic Features: 

Late onset gait abnormalities associated with MRI documented vermis atrophy have been reported in a single autosomal dominant pedigree.  The diagnosis of CFEOM1 was confirmed with molecular studies but only two older individuals aged 79 and 53 years had the cerebellar atrophy while a 33 year old in the same family had only CFEOM with no gait difficulties and no neuroimaging abnormalities.

Genetics

CFEOM1 is an autosomal dominant disorder caused by mutations in the KIF21A gene located at 12q12.  This is considered the classic form of congenital, restrictive strabismus but other types such as CFEOM2 (602078) and CFEOM3 (600638, 609384) have also been reported.  CFEOM3 is a clinically heterogeneous autosomal dominant condition and the label is usually applied to individuals who do not meet the criteria for the other two types.  A rare subtype (CFEOM3B) is also due to mutations in the KIF21A gene.  CFEOM3A (600638) is caused by mutations in the TUBB3 gene (16q24) while CFEOM3C (609384) maps to 13q.

The CFEOM2 (602078) phenotype is due to mutations in the PHOX2A (ARIX) gene and inherited in an autosomal recessive pattern.

Other nonsyndromal forms of congenital fibrosis of extraocular muscles include: CFEOM3C (609384), CFEOM5 (616219), and CFEOM with synergistic divergence (609612).  See also Tukel CFEOM syndrome (609428).

Pedigree: 
Autosomal dominant
Treatment
Treatment Options: 

Normal ocular movements cannot be restored but large recessions of the inferior recti followed by frontalis suspension of the upper eyelids can improve severe ptosis and the compensatory chin-up gaze. Corneal lubrication must be maintained.  Refractive errors and amblyopia should be corrected.  

References
Article Title: 

Fibrosis of Extraocular Muscles, CFEOM2

Clinical Characteristics
Ocular Features: 

This is a congenital, autosomal recessive, nonprogressive type of CFEOM which has been described in several consanguineous Middle Eastern families.  The responsible mutations are in a different gene than the one responsible for autosomal dominant CFEOM1 cases although some of the clinical features are similar.  However, in CFEOM2 the eyes are less likely to be infraducted and instead are often fixed in extreme abduction.  In addition, the phenotype is more variable with some eyes fixed in the 'neutral' position and others having more mobility than usually seen in CFEOM1 but the clinical heterogeneity is less than that seen in CFEOM3.  Ptosis is part of both phenotypes.  All patients have severe restrictions in ocular motility.  It has been suggested that CEFOM2 patients are likely to have involvement of both superior and inferior divisions of the oculomotor nerve whereas only the superior division is abnormal in CFEOM1.  Binocular vision is absent and amblyopia is common.  The pupils may be small and respond poorly to light. Refractive errors are common.

Based on visual field testing and ERG findings, it has been suggested that subnormal vision in CFEOM2 may be due to undescribed retinal dysfunction.  

Systemic Features: 

Mild facial muscle weakness may be apparent. 

Genetics

This is an autosomal recessive disorder caused by homozygous mutations in the PHOX2A gene at 11q13.3-q13.4.  Another more common form of CFEOM is the autosomal dominant CFEOM1 type (135700) in which the primary fixed deviation is infraduction. The third type is CFEOM3 (600638, 609384) which is clinically more heterogeneous. 

Other nonsyndromal forms of congenital fibrosis of extraocular muscles include: CFEOM3C (609384), CFEOM5 (616219), and CFEOM with synergistic divergence (609612).  See also Tukel CFEOM syndrome (609428).

Pedigree: 
Autosomal recessive
Treatment
Treatment Options: 

Restoration of normal ocular motility is difficult but cosmetic improvement is possible by correcting some of the ptosis with frontalis slings.  Corneal lubrication must be maintained and amblyopia should be treated. 

References
Article Title: 

Adrenoleukodystrophy, Autosomal

Clinical Characteristics
Ocular Features: 

This early onset and rapidly progressive form of adrenoleukodystrophy is rare.  The early onset and rapidly fatal course of the disease has limited full delineation of the ocular features.  The most striking is the presence of 'leopard-spots' pigmentary changes in the retina.  Polar cataracts, strabismus, and epicanthal folds have also been reported. 

Systemic Features: 

Onset of symptoms occurs shortly after birth often with seizures and evidence of psychomotor deficits.  Rapid neurologic deterioration begins at about 1 year of age with death usually by the age of 3 years.  Hyperpigmentation of the skin may be apparent a few months after birth.  Opisthotonus has been observed.  The ears may be low-set, the palate is highly arched, and the nostrils anteverted.  Frontal bossing may be present.  Serum pipecolic acid and very-long-chain fatty acids (VLCFAs) can be markedly elevated.  Cystic changes in the kidneys have been reported. 

Genetics

This is an autosomal recessive peroxismal disorder resulting from homozygous mutations in receptor gene mutations such as PEX1, PEX5, PEX13, and PEX26.

There is also an X-linked recessive adrenoleukodystrophy (300100) sometimes called ALD but it lacks some of the morphologic features and is somewhat less aggressive. 

Neonatal adrenoleukodystrophy along with infantile Refsum disease (266510, 601539) and Zellweger syndrome (214100) are now classified as Zellweger spectrum or perioxismal biogenesis disorders.

Pedigree: 
Autosomal recessive
Treatment
Treatment Options: 

Treatment is mainly supportive for associated health problems. 

References
Article Title: 

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

Albinism, Oculocutaneous, Type IV

Clinical Characteristics
Ocular Features: 

The ocular manifestations in type IV oculocutaneous albinism are similar to those of other types.  Nystagmus, strabismus, misrouting of neuronal axons, and foveal hypoplasia are prominent features although there is some clinical heterogeneity among patients.  Nystagmus may not be present at birth but is almost always evident by 3-4 months of age.  The iris may be pale blue or tan and does not generally darken with age.  Poor stereopsis is common.  Vision is stable after childhood and usually in the range of 20/100-20/400. 

Systemic Features: 

Hair color is generally intermediate between white and brown but many patients have only white hair and in others the hair is brown.  Little darkening occurs as patients become older.  The skin is often white or creamy yellow. 

Genetics

This type of oculocutaneous albinism is one of the more common types found among Japanese and maybe Chinese individuals although it has also been reported in German and Turkish individuals.  This is a rare autosomal recessive form of albinism caused by mutations in the MATP (SLC45A2) gene located at 5p13.3. 

A single Japanese family with 16 affected members has been reported in which the transmission pattern was consistent with autosomal dominant inheritance. Heterozygous mutations in the SLC45A2 gene segregated appropriately.

Other types include OCA1 (203100, 606952 ), OCA2 (203200 ), OAC3 (203290), OAC5 (615179), and OCA6 (113750)..

Pedigree: 
Autosomal dominant
Autosomal recessive
Treatment
Treatment Options: 

There is no treatment for the hypopigmentation.  Low vision aids and tinted lenses may help some patients.  Exposure to the sun should be limited. 

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

Albinism, Oculocutaneous, Type II

Clinical Characteristics
Ocular Features: 

The iris and retina lack normal pigmentation and translucency of the iris can be demonstrated.  Anomalous decussation of neuronal axons in the chiasm and foveal hypoplasia result in decreased visual acuity.  Vision loss into the range of 20/100-20/200 does not progress after early childhood but is sometimes as good as 20/30.   Nystagmus is often present from about 3-4 months of age although it is less severe than in type I oculocutaneous albinism (203100, 606952).  The iris may darken to some extent with age.  Strabismus has been reported.  Significant refractive errors are often present and stereopsis is reduced.  The VEP responses are altered and can be used to document abnormal chiasmal decussation. 

Systemic Features: 

Melanin pigment is reduced in the skin and hair as well as the eyes.  Individuals at birth may be misdiagnosed as OCA type I but it is common for pigmentation to increase in older individuals resulting in yellow or reddish-blond hair and the appearance of freckles and nevi.  The skin may be creamy-white but this is often not as striking as in OCAI.  It is possible for tanning to take place in some patients.  This condition in Africans or African Americans is sometimes called brown oculocutaneous albinism (BOCA).  There is an increased risk of skin cancer of all types. 

Genetics

Type II is the most common type of oculocutaneous albinism and is especially prevalent among individuals of African heritage and in several Native American populations.  It is an autosomal recessive condition caused by homozygous 2.7 kb deletions in the OCA2 gene (15q24.3-q12).  Heterozygotes have normal pigmentation. 

Oculocutaneous albinism type I (203100, 606952) is a separate disorder with many similar features caused by mutations in the TYR gene.  Other types of autosomal recessive albinism are OCA3 (203290 ), and OCA4 (606574). 

Pedigree: 
Autosomal recessive
Treatment
Treatment Options: 

No treatment is available for the hypopigmentation.  Low vision aids can be helpful. Significant refractive errors should, of course, be corrected and dark lenses may be helpful during outdoor activities. The skin should be protected from excessive sun exposure. 

References
Article Title: 

Vision in albinism

Summers CG. Vision in albinism. Trans Am Ophthalmol Soc. 1996;94:1095-155.

PubMed ID: 
8981720

Oculocutaneous albinism

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

PubMed ID: 
17980020

Hermansky-Pudlak Syndrome

Clinical Characteristics
Ocular Features: 

Oculocutaneous hypopigmentation is common to all types of HPS.  The ocular manifestations are similar to that of other types of albinism.  Iris transillumination defects, nystagmus, and strabismus are common features.   Visual acuity is usually stable in the range of 20/40-20/300 and often accompanied by photophobia.  Foveal hypoplasia and fundus hypopigmentation are present similar to that found in other hypopigmentation disorders.  The same is true of excessive decussation of retinal neuron axons at the chiasm.  Many patients have significant refractive errors. 

Systemic Features: 

In addition to decreased hair, ocular, and skin pigmentation, HPS patients suffer from bleeding diathesis, platelet deficiencies, and accumulation of ceroid material in lysosomes.  Pigment can be found in large amounts in reticuloendothelial cells and in the walls of small blood vessels.  Some of the same features are found in Chediak-Higashi  syndrome (214500) which, however, has additional qualitative changes in leukocytes.   HPS2 differs from other forms of HPS in having immunodeficiency and congenital neutropenia.  Some patients, especially those with HPS1 and HPS4 mutations, have restrictive lung disease secondary to pulmonary fibrosis often causing symptoms in the third and fourth decades of life.  Others have granulomatous colitis, kidney failure, and cardiomyopathy.  Solar skin damage is a risk with actinic keratosis, nevi, lentigines and basal cell carcinoma seen in many patients.

Bleeding time is prolonged secondary to an impairment of the normal aggregation response of platelets.  Easy bruising, epistaxis, prolonged bleeding during menstruation, after tooth extraction, and after minor surgical procedures are often reported.  Platelets lack the normal number of 'dense bodies'.  Coagulation factor activity and platelet counts are normal.

The amount of hair and skin pigmentation is highly variable.  Some patients are so lightly pigmented that they are misdiagnosed as having tyrosinase-negative albinism while others have yellow to brown hair with irides blue to hazel.  Some darkening of hair is common. 

Genetics

This is an autosomal recessive genetically heterogeneous condition resulting from mutations in at least 12 loci: HPS1 (203300) at 10q23.1-q23.2, AP3B1 causing HPS2 (608233) at 5q14.1, and AP3D1 (617050) at 19p13.3 causing HPS 10, whereas in types HPS3 (606118) at 3q24, HPS4 (606682) at 22q11.2-q12.2, HPS5 (607521) at 11p15-p13, HPS6 (607522) at 10q24.32 the mutations themselves have not been characterized.  HPS7 is caused by mutations in the DTNBP1 gene (607145) located at locus 6p22.3 and HPS8 by mutations in the BLOC1S3 gene (609762) at 19q13.  The nature of the mutations is variable and often unique to the population in which they are found. 

Chediak-Higashi  syndrome (214500) is a somewhat similar disorder but with leukocyte abnormalities and results from a different gene mutation.

Pedigree: 
Autosomal recessive
Treatment
Treatment Options: 

It has been suggested that any patients with pigmentation disorders should be asked about bleeding problems to rule out HPS.  A hematologic consultation should be obtained if necessary, especially before elective surgery, to avoid bleeding complications through the use of appropriate preoperative measures.   Low vision aids can be helpful.  The skin should be protected from sunburn.  Lifelong surveillance is required for ocular and systemic problems.  The use of aspirin and indomethacin should be avoided. 

References
Article Title: 

Mutations in AP3D1 associated with immunodeficiency and seizures define a new type of Hermansky-Pudlak syndrome

Ammann S, Schulz A, Krageloh-Mann I, Dieckmann NM, Niethammer K, Fuchs S, Eckl KM, Plank R, Werner R, Altmuller J, Thiele H, Nurnberg P, Bank J, Strauss A, von Bernuth H, Zur Stadt U, Grieve S, Griffiths GM, Lehmberg K, Hennies HC, Ehl S. Mutations in AP3D1 associated with immunodeficiency and seizures define a new type of Hermansky-Pudlak syndrome. Blood. 2016 Feb 25;127(8):997-1006.

PubMed ID: 
26744459

Optic Nerve Hypoplasia, Bilateral

Clinical Characteristics
Ocular Features: 

The hallmark of this syndrome is bilateral optic nerve dysplasia including aplasia and hypoplasia. It may occur in isolation or as part of other syndromes, especially in those having abnormalities of the central nervous system.  All components of the nerve head are abnormally small including the entire disc area, the cup, and the neuroretinal rim. It has been reported that retinal vein tortuosity is predictive of patients with endocrinopathies.  Retinal arteries often appear straight and narrow but this may not be seen in all cases.  Visual acuity ranges from 20/50 to NLP but usually 20/200 or better.  Many patients have nystagmus and strabismus.

This disorder shares many characteristics with septooptic dysplasia (182230) but the optic nerve anomalies are usually unilateral in the latter disorder and the disc rim often has a double margin.  Mutations in different genes are responsible for the two disorders. 

Systemic Features: 

Pituitary dysfunction and endocrinopathy may lead to life-threatening illness caused by adrenal crisis or hypoglycemia.  An absent or abnormal septum pellucidum is present in 49% of patients and 64% have a hypothalamic-pituitary axis abnormality.  Among those with an abnormal septum pellucidum, 56% have some kind of endocrinopathy. Other midline brain defects and cerebral anomalies have also been reported.

 

Genetics

Bilateral optic nerve hypoplasia is inherited in an autosomal dominant pattern based on the few families reported.  Mutations in the PAX6 (11q13) gene are responsible.

A somewhat similar disease with extensive CNS and endocrinological abnormalities is septooptic dysplasia (182230) caused by mutations in the HESX1 gene. 

Pedigree: 
Autosomal dominant
Treatment
Treatment Options: 

There is no treatment for the optic nerve hypoplasia but individuals need to be monitored for endocrinopathy and treated appropriately.  Low vision aids and sometimes mobility training can be helpful for some patients. 

References
Article Title: 

Endocrine status in patients with optic nerve hypoplasia: relationship to midline central nervous system abnormalities and appearance of the hypothalamic-pituitary axis on magnetic resonance imaging

Birkebaek NH, Patel L, Wright NB, Grigg JR, Sinha S, Hall CM, Price DA, Lloyd IC, Clayton PE. Endocrine status in patients with optic nerve hypoplasia: relationship to midline central nervous system abnormalities and appearance of the hypothalamic-pituitary axis on magnetic resonance imaging. J Clin Endocrinol Metab. 2003 Nov;88(11):5281-6.

PubMed ID: 
14602752

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