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In the adult and juvenile forms of open-angle glaucoma, vision loss begins at the periphery (outer edges) of the visual field, resulting in tunnel vision. Because the visual loss in not in the individual's central vision, they may not notice this change. However, if the glaucoma is left untreated, loss of vision progresses and the central vision is often affected, sometimes resulting in blindness. The average time from development of high eye fluid pressures to the appearance of visual loss is 18 years in the adult form, but much shorter in the juvenile form.
In contrast to the adult and juvenile forms, congenital or infantile open-angle glaucoma is noted at birth or
|Types of glaucoma and related genetic information|
|Disorder||Alternative names||Inheritance||Abnormal protein||Abnormal gene||Gene location|
|Glaucoma 1, open angle, A (GLC1A)||Juvenile onset primary open-angle glaucoma; Hereditary juvenile glaucoma||Autosomal dominant||Trabecular meshwork-induced glucocorticoid response protein (myocilin)||MYOC, (also known as TIGR, GLC1A, JOAG, GPOA)||1q24.3–q25.2;|
|Glaucoma 1, open angle, B (GLC1B)||Adult onset primary open-angle glaucoma; Hereditary adult glaucoma||Autosomal dominant||Unknown||Unknown||2qcen–q13; (additional loci under investigation)|
|Glaucoma 1, open angle, C (GLC1C)||Adult onset primary open-angle glaucoma; Hereditary adult glaucoma||Autosomal dominant||Unknown||Unknown||3q21–q24|
|Glaucoma 1, open angle, D (GLC1D)||Adult onset primary open-angle glaucoma; Hereditary adult glaucoma||Autosomal dominant||Unknown||Unknown||8q23|
|Glaucoma 1, open angle, E (GLC1E)||Adult onset primary open-angle glaucoma; Hereditary adult glaucoma||Autosomal dominant||Unknown||Unknown||10p15–p14|
|Glaucoma 1, open angle, F (GLC1F)||Adult onset primary open-angle glaucoma; Hereditary adult glaucoma||Autosomal dominant||Unknown||Unknown||7q35–36|
|Glaucoma 3, primary infantile, A (GLC3A)||Congenital glaucoma; Buphthalmos||Autosomal recessive||Cytochrome P4501B1||CYP1B1||2p22–p21|
|Glaucoma 3, primary infantile, B (GLC3B)||Congenital glaucoma||Autosomal recessive||Unknown||Unknown||1p36.2–36.1|
|Iridogoniodysgenesis, type 1 (IRID1)||Iridogoniodysgenesis anomaly; familial glaucomaIridogoniodysplasia||Autosomal dominant||Forkhead Transcription factor||FKHL7||6P25|
|Iridogoniodysgenesis, type 2 (IRID1)||Iridogoniodysgenesis anomaly; Iris hypoplasia with early-onset glaucoma||Autosomal dominant||Paired-like homeodomain transcription factor-2||PITX2 (also known as; IDG2, RIEG1, RGS, IGDS2)||4q25–q26|
|Rieger syndrome, type 1 (RIEG1)||Iridogoniodysgenesis with Somatic anomalies||Autosomal dominant||Paired-like homeodomain transcription factor-2||PITX2 (also known as; IDG2, RIEG1, RGS, IGDS2)||4q25–q26|
|Rieger syndrome, type 2 (RIEG2)||Iridogoniodysgenesis with Somatic anomalies||Autosomal dominant||Unknown||Unknown||13q14|
|Glaucoma-related pigment dispersion syndrome (GPDS1)||Pigment dispersion syndrome and pigmentary glaucoma||Autosomal dominant||Unknown||Unknown||7q35–q36|
within the first three years of life. Symptoms include cloudy corneas, excessive tearing, and sensitivity to light. Because the eye is very flexible in infants, increased fluid pressure may cause bulging of the eye (buphthalmos, or "ox eye"). Children with glaucoma in only one eye are usually diagnosed earlier because a difference in eye size can be noticed. When the disorder affects both eyes, many parents view the large eyes as attractive and do not seek help until other symptoms develop, delaying the diagnosis.
With closed-angle glaucoma, symptoms come on suddenly. People may experience blurred vision, severe pain, headache, sensitivity to light, and nausea. The development of this type of glaucoma is an emergency and requires immediate treatment.
Author Info: Oren Traub MD, PhD, The Gale Group Inc., Gale, Detroit, Gale Encyclopedia of Genetic Disorders Part I, 2002
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