Conditions listing Norrie Disease as a symptom may also be potential underlying causes of Norrie Disease. Our database lists the following as having Norrie Disease as a symptom of that condition:
As with all medical conditions, there may be many causal factors. Further relevant information on causes of Norrie Disease may be found in:
16 MEDICAL BOOKS ONLINE! Review excerpts from medical books online, free, without registration, for more information about the causes of Norrie Disease.
Transient vision loss (<24 hours)
Source: In a Page: Signs and Symptoms, 2004
Source: In A Page: Pediatric Signs and Symptoms, 2007
With amaurosis fugax, recurrent attacks of unilateral vision loss may last from a few seconds to a few minutes. Vision is normal at other times. Transient unilateral weakness, hypertension, and elevated intraocular pressure (IOP) in the affected eye may also occur.
Typically, painless and gradual visual blurring precedes vision loss. As the cataract progresses, the pupil turns milky white.
Immediately or shortly after blunt head trauma, vision may be blurred, double, or lost. Generally, vision loss is temporary. Other findings include headache, anterograde and retrograde amnesia, transient loss of consciousness, nausea, vomiting, dizziness, irritability, confusion, lethargy, and aphasia.
Retinal edema and hemorrhage lead to visual blurring, which may progress to blindness.
Typically, endophthalmitis — an intraocular inflammation — follows penetrating trauma, I.V. drug use, or intraocular surgery, causing possibly permanent unilateral vision loss; a sympathetic inflammation may affect the other eye.
Glaucoma produces gradual visual blurring that may progress to total blindness. Acute angle-closure glaucoma is an ocular emergency that may produce blindness within 3 to 5 days. Findings are rapid onset of unilateral inflammation and pain, pressure over the eye, moderate pupil dilation, nonreactive pupillary response, a cloudy cornea, reduced visual acuity, photophobia, and perception of blue or red halos around lights. Nausea and vomiting may also occur.
Chronic angle-closure glaucoma has a gradual onset and usually produces no symptoms, although blurred or halo vision may occur. If untreated, it progresses to blindness and extreme pain.
Chronic open-angle glaucoma is usually bilateral, with an insidious onset and a slowly progressive course. It causes peripheral vision loss, aching eyes, halo vision, and reduced visual acuity (especially at night).
Following eye injury, sudden unilateral or bilateral vision loss may occur. Vision loss may be total or partial and permanent or temporary. The eyelids may be reddened, edematous, and lacerated; intraocular contents may be extruded.
Degeneration of the optic nerve, optic atrophy can develop spontaneously or follow inflammation or edema of the nerve head, causing irreversible loss of the visual field with changes in color vision. Pupillary reactions are sluggish, and optic disk pallor is evident.
An umbrella term for inflammation, degeneration, or demyelinization of the optic nerve, optic neuritis usually produces temporary but severe unilateral vision loss. Pain around the eye occurs, especially with movement of the globe. This may occur with visual field defects and a sluggish pupillary response to light. Ophthalmoscopic examination commonly reveals hyperemia of the optic disk, blurred disk margins, and filling of the physiologic cup.
Bilateral vision loss may develop as a result of bony impingements on the cranial nerves. This occurs with hearing loss, tinnitus, vertigo, and severe, persistent bone pain. Cranial enlargement may be noticeable frontally and occipitally, and headaches may occur. Sites of bone involvement are warm and tender, and impaired mobility and pathologic fractures are common.
As a pituitary adenoma grows, blurred vision progresses to hemianopia and, possibly, unilateral blindness. Double vision, nystagmus, ptosis, limited eye movement, and headaches may also occur.
Retinal artery occlusion is a painless ocular emergency that causes sudden unilateral vision loss, which may be partial or complete. Pupil examination reveals a sluggish direct pupillary response and a normal consensual response. Permanent blindness may occur within hours.
Depending on the degree and location of detachment, painless vision loss may be gradual or sudden and total or partial. Macular involvement causes total blindness.
With partial vision loss, the patient may describe visual field defects or a shadow or curtain over the visual field as well as visual floaters.
Most common in geriatric patients, retinal vein occlusion — a painless disorder — causes a unilateral decrease in visual acuity with variable vision loss. IOP may be elevated in both eyes.
Rift Valley fever is a viral disease that causes inflammation of the retina and may result in some permanent vision loss. Typical signs and symptoms include fever, myalgia, weakness, dizziness, and back pain. A small percentage of patients may develop encephalitis or may progress to hemorrhagic fever that can lead to shock and hemorrhage.
Occurring in elderly patients, senile macular degeneration causes painless blurring or loss of central vision. Vision loss may proceed slowly or rapidly, eventually affecting both eyes. Visual acuity may be worse at night.
Corneal scarring from associated conjunctival lesions produces marked vision loss. Purulent conjunctivitis, eye pain, and difficulty opening the eyes occur. Additional findings include widespread bullae, fever, malaise, cough, drooling, inability to eat, sore throat, chest pain, vomiting, diarrhea, myalgias, arthralgias, hematuria, and signs of renal failure.
Vision loss and visual blurring with a throbbing, unilateral headache characterize this disorder. Other findings include malaise, anorexia, weight loss, weakness, low-grade fever, generalized muscle aches, and confusion.
With vitreous hemorrhage, sudden unilateral vision loss may result from intraocular trauma, ocular tumors, or systemic disease (especially diabetes, hypertension, sickle cell anemia, or leukemia). Visual floaters and partial vision with a reddish haze may occur. The patient’s vision loss may be permanent.
Chloroquine therapy may cause patchy retinal pigmentation that typically leads to blindness. Phenylbutazone may cause vision loss and increased susceptibility to retinal detachment. Digoxin, indomethacin, ethambutol, quinine sulfate, and methanol toxicity may also cause vision loss.
Source: Handbook of Signs & Symptoms (Third Edition), 2006
In this disorder, recurrent attacks of unilateral vision loss may last from a few seconds to a few minutes. Vision is normal at other times. Other findings may include transient unilateral weakness, hypertension, and elevated intraocular pressure (IOP) in the affected eye.
Typically, painless and gradual visual blurring precedes vision loss. As the cataract progresses, the pupil turns milky white.
Immediately or shortly after blunt head trauma, the patient may develop blurred, double, or lost vision. Vision loss is usually temporary. Other findings include headache, anterograde and retrograde amnesia, transient loss of consciousness, nausea, vomiting, dizziness, irritability, confusion, lethargy, and aphasia.
Some corneal dystrophies cause vision loss with associated pain, photophobia, tearing, and corneal opacities.
Retinal edema and hemorrhage lead to visual blurring, which may progress to blindness.
Typically, this intraocular inflammation follows penetrating trauma, I.V. drug use, or intraocular surgery, causing unilateral vision loss that may be permanent; a sympathetic inflammation may affect the other eye.
This disorder produces gradual visual blurring that may progress to total blindness. Acute angle-closure glaucoma is an ocular emergency that may produce blindness within 3 to 5 days. It’s characterized by rapid onset of unilateral inflammation and pain, pressure over the eye, moderate pupil dilation, nonreactive pupillary response, a cloudy cornea, reduced visual acuity, photophobia, and perception of blue or red halos around lights. Nausea and vomiting may also occur.
Chronic angle-closure glaucoma has a gradual onset and usually produces no symptoms, although blurred or halo vision may occur. If untreated, it progresses to blindness and extreme pain.
Chronic open-angle glaucoma usually has an insidious onset, progresses slowly, and affects both eyes. It causes peripheral vision loss, aching eyes, halo vision, and reduced visual acuity (especially at night).
When this disorder affects the nasociliary nerve, bilateral vision loss is accompanied by eyelid lesions, conjunctivitis, skin lesions (usually on the nose), and ocular muscle palsies.
Blood in the anterior chamber can reduce vision to light perception only. Most hyphemas are the direct result of blunt trauma to the normal eye.
This inflammation of the cornea may lead to complete unilateral vision loss. Other findings include an opaque cornea, increased tearing, irritation, and photophobia.
Sudden unilateral or bilateral vision loss may occur after an eye injury. Vision loss may be total or partial and permanent or temporary. The eyelids may be reddened, edematous, and lacerated; intraocular contents may be extruded.
Degeneration of the optic nerve, optic atrophy can develop spontaneously or follow inflammation or edema of the nerve head, causing irreversible loss of the visual field with changes in color vision. Pupillary reactions are sluggish, and optic disk pallor is evident.
An umbrella term for inflammation, degeneration, or demyelinization of the optic nerve, optic neuritis usually produces temporary but severe unilateral vision loss, pain around the eye (especially with movement of the globe), a sluggish pupillary response to light and, possibly, visual field defects. Ophthalmoscopic examination commonly reveals hyperemia of the optic disk, blurred disk margins, and filling of the physiologic cup.
In this disorder, bony impingements on the cranial nerves may cause bilateral vision loss, which may be accompanied by hearing loss, tinnitus, vertigo, and severe, persistent bone pain. Cranial enlargement may be noticeable frontally and occipitally, and headaches may occur. Sites of bone involvement are warm and tender, and impaired mobility and pathologic fractures are common.
Papilledema is characterized by swelling of both optic disks from increased intracranial pressure. Acute papilledema may lead to momentary blurring or transiently obscured vision, whereas chronic papilledema may lead to vision loss.
As a pituitary adenoma grows, blurred vision progresses to hemianopia and, possibly, unilateral blindness. Double vision, nystagmus, ptosis, limited eye movement, and headaches may also occur.
This painless ocular emergency causes sudden unilateral vision loss, which may be partial or complete. Pupil examination reveals a sluggish direct pupillary response and a normal consensual response. Permanent blindness may occur within hours.
Depending on the degree and location of detachment, painless vision loss may be gradual or sudden and total or partial. Macular involvement causes total blindness. Other effects include visual floaters, light flashes, and a sensation of a shadow or curtain over the visual field.
Most common in geriatric patients, this painless disorder causes a unilateral decrease in visual acuity with variable vision loss. IOP may be elevated in both eyes.
Inflammation of the retina is a complication of this viral disease that may result in some degree of permanent vision loss. Typical signs and symptoms include fever, myalgia, weakness, dizziness, and back pain. A small percentage of patients may develop encephalitis or hemorrhagic fever that can lead to shock and hemorrhage.
Occurring in elderly patients, this disorder causes painless blurring or loss of central vision. Vision loss may proceed slowly or rapidly, eventually affecting both eyes. Visual acuity may be worse at night.
Corneal scarring from associated conjunctival lesions produces marked vision loss, which may be accompanied by purulent conjunctivitis, eye pain, and difficulty opening the eyes. Additional findings include widespread bullae, fever, malaise, cough, drooling, inability to eat, sore throat, chest pain, vomiting, diarrhea, myalgia, arthralgia, hematuria, and signs of renal failure.
Vision loss and visual blurring with a throbbing, unilateral headache characterize this disorder. Other findings include malaise, anorexia, weight loss, weakness, low-grade fever, generalized muscle aches, and confusion.
This rare disorder may initially produce varying degrees of vision loss and a mild infection resembling bacterial conjunctivitis. Conjunctival follicles, red and edematous eyelids, pain, photophobia, tearing, and exudation also occur. After about 1 month, conjunctival follicles enlarge into inflamed yellow or gray papillae.
Inflammation of the uveal tract may result in unilateral vision loss. Anterior uveitis produces moderate to severe eye pain, severe conjunctival injection, photophobia, and a small, nonreactive pupil. Posterior uveitis may produce insidious onset of blurred vision, conjunctival injection, visual floaters, pain, and photophobia. Associated posterior scar formation distorts the shape of the pupil.
This condition, which may result from intraocular trauma, ocular tumors, or systemic disease (especially diabetes, hypertension, sickle cell anemia, or leukemia), can cause sudden unilateral vision loss, visual floaters, and a reddish haze. The vision loss may be permanent.
Chloroquine therapy may cause patchy retinal pigmentation that typically leads to blindness. Digoxin derivatives, indomethacin, ethambutol, quinine sulfate, and methanol toxicity may also cause vision loss.
Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
With this amaurosis fugax, recurrent attacks of unilateral vision loss may last from a few seconds to a few minutes. Vision is normal at other times. Transient unilateral weakness, hypertension, and elevated IOP in the affected eye may also occur.
ALERT: Acute angle-closure glaucoma is an ocular emergency that may produce blindness within 3 to 5 days.
Chronic angle-closure glaucoma has a gradual onset and usually produces no symptoms, although blurred or halo vision may occur. If untreated, it progresses to blindness and extreme pain.
Chronic open-angle glaucoma is usually bilateral, with an insidious onset and a slowly progressive course. It causes peripheral vision loss, aching eyes, halo vision, and reduced visual acuity (especially at night).
Some dystrophies cause vision loss with associated pain, photophobia, tearing, and corneal opacities.
When herpes zoster affects the nasociliary nerve, bilateral vision loss is accompanied by eyelid lesions, conjunctivitis, skin lesions that usually appear on the nose, and ocular muscle palsies.
Blood in the anterior chamber can reduce vision to light perception only. Most hyphemas are the direct result of blunt trauma to the normal eye.
An inflammation of the cornea, keratitis may lead to complete unilateral vision loss. Other findings include an opaque cornea, increased tearing, irritation, and photophobia.
Following eye injury, sudden unilateral or bilateral vision loss may occur. Vision loss may be total or partial and permanent or temporary. The eyelids may be reddened, edematous, and lacerated; intraocular contents may be extruded.
Degeneration of the optic nerve, optic atrophy can develop spontaneously or follow inflammation or edema of the nerve head, causing irreversible loss of the visual field with changes in color vision. Pupillary reactions are sluggish, and optic disk pallor is evident.
An umbrella term for inflammation, degeneration, or demyelinization of the optic nerve, optic neuritis usually produces temporary but severe unilateral vision loss. Pain around the eye occurs, especially with movement of the globe. This may occur with visual field deficits and a sluggish pupillary response to light. Ophthalmoscopic examination commonly reveals hyperemia of the optic disk, blurred disk margins, and filling of the physiologic cup.
Bilateral vision loss may develop as a result of bony impingements on the cranial nerves. This occurs with hearing loss, tinnitus, vertigo, and severe, persistent bone pain. Cranial enlargement may be noticeable frontally and occipitally, and headaches may occur. Sites of bone involvement are warm and tender, and impaired mobility and pathologic fractures are common.
Papilledema is characterized by swelling of the optic disk from increased intracranial pressure; both optic disks are affected. Acute papilledema may lead to momentary blurring or transiently obscured vision, whereas chimeric papilledema may lead to vision loss.
As a pituitary adenoma grows, blurred vision progresses to hemianopia and, possibly, unilateral blindness. Double vision, nystagmus, ptosis, limited eye movement, and headaches may also occur.
A painless ocular emergency, retinal artery occlusion causes sudden unilateral vision loss, which may be partial or complete. Pupil examination reveals a sluggish direct pupillary response and a normal consensual response. Permanent blindness may occur within hours.
Depending on the degree and location of detachment, painless vision loss may be gradual or sudden and total or partial. Macular involvement causes total blindness.
With partial vision loss, the patient may describe visual field deficits or a shadow or curtain over the visual field as well as visual floaters.
Most common in elderly patients, retinal vein occlusion is a painless disorder that causes a unilateral decrease in visual acuity with variable vision loss. IOP may be elevated in both eyes.
A viral disease, Rift Valley fever causes inflammation of the retina and may result in some permanent vision loss. Typical signs and symptoms include fever, myalgia, weakness, dizziness, and back pain. A small percentage of patients may develop encephalitis or may progress to hemorrhagic fever that can lead to shock and hemorrhage.
Occurring in elderly patients, senile macular degeneration causes painless blurring or loss of central vision. Vision loss may proceed slowly or rapidly, eventually affecting both eyes. Visual acuity may be worse at night.
Corneal scarring from associated conjunctival lesions produces marked vision loss. Purulent conjunctivitis, eye pain, and difficulty opening the eyes occur. Additional findings include widespread bullae, fever, malaise, cough, drooling, an inability to eat, sore throat, chest pain, vomiting, diarrhea, myalgia, arthralgia, hematuria, and signs of renal failure.
Vision loss and visual blurring with a throbbing, unilateral headache characterize temporal arteritis. Other findings include malaise, anorexia, weight loss, weakness, low-grade fever, generalized muscle aches, and confusion.
A rare disorder, trachoma may initially produce varying vision loss and a mild infection resembling bacterial conjunctivitis. Conjunctival follicles, red and edematous eyelids, pain, photophobia, tearing, and exudation also occur. After about 1 month, conjunctival follicles enlarge into inflamed yellow or gray papillae.
Inflammation of the uveal tract may result in unilateral vision loss. Anterior uveitis produces moderate to severe eye pain, severe conjunctival injection, photophobia, and a small, nonreactive pupil. Posterior uveitis may produce an insidious onset of blurred vision, conjunctival injection, visual floaters, pain, and photophobia. Associated posterior scar formation distorts the shape of the pupil.
With vitreous hemorrhage, sudden unilateral vision loss may result from intraocular trauma, ocular tumors, or systemic disease (especially diabetes, hypertension, sickle cell anemia, or leukemia). Visual floaters and partial vision with a reddish haze may occur. The vision loss may be permanent.
Chloroquine therapy may cause patchy retinal pigmentation that typically leads to blindness. Phenylbutazone may cause vision loss and increased susceptibility to retinal detachment. Digoxin, indomethacin, ethambutol, quinine sulfate, and methanol toxicity may also cause visual disturbances and possibly vision loss.
Source: Alarming Signs and Symptoms: Lippincott Manual of Nursing Practice Series, 2007
With amaurosis fugax, recurrent attacks of unilateral vision loss may last from a few seconds to a few minutes. Vision is normal at other times. Transient unilateral weakness, hypertension, and elevated intraocular pressure (IOP) in the affected eye may also occur.
With a cataract, usually, painless and gradual visual blurring precedes vision loss. As the cataract progresses, the pupil turns milky white. Night blindness and halo vision may be early signs of this disorder.
Immediately or shortly after blunt head trauma, which causes a concussion, vision may be blurred, double, or lost. Generally, vision loss is temporary. Other findings include headache, anterograde and retrograde amnesia, transient loss of consciousness, nausea, vomiting, dizziness, irritability, confusion, lethargy, and aphasia.
With diabetic retinopathy, retinal edema and hemorrhage lead to visual blurring, which may progress to blindness. The patient may also have a loss of central vision and color vision.
Typically, endophthalmitis follows penetrating trauma, I.V. drug use, or intraocular surgery, causing possibly permanent unilateral vision loss; a sympathetic inflammation may affect the other eye. The patient with endophthalmitis may also experience headache, photophobia, and ocular discharge.
Glaucoma produces gradual visual blurring that may progress to total blindness. Acute angle-closure glaucoma is an ocular emergency that may produce blindness within 3 to 5 days. Findings are rapid onset of unilateral inflammation and pain, pressure over the eye, moderate pupil dilation, nonreactive pupillary response, a cloudy cornea, reduced visual acuity, photophobia, and perception of blue or red halos around lights. Nausea and vomiting may also occur.
Chronic open-angle glaucoma is usually bilateral, with an insidious onset and a slowly progressive course. It causes peripheral vision loss, aching eyes, halo vision, and reduced visual acuity (especially at night).
When herpes zoster affects the nasociliary nerve, bilateral vision loss is accompanied by eyelid lesions, conjunctivitis, skin lesions that usually appear on the nose, and ocular muscle palsies.
With a hyphema, blood in the anterior chamber can reduce vision to light perception only. Other effects include moderate pain, conjunctival injection, and eyelid edema. Most hyphemas are the direct result of blunt trauma to the normal eye.
Keratitis (inflammation of the cornea) may lead to complete unilateral vision loss. Other findings include an opaque cornea, increased tearing, irritation, and photophobia.
Following eye injury, sudden unilateral or bilateral vision loss may occur. Vision loss may be total or partial and permanent or temporary. The eyelids may be reddened, edematous, and lacerated; intraocular contents may be extruded.
Optic atrophy (degeneration of the optic nerve) can develop spontaneously or follow inflammation or edema of the nerve head, causing irreversible loss of the visual field with changes in color vision. Pupillary reactions are sluggish, and optic disk pallor is evident.
Optic neuritis usually produces temporary but severe unilateral vision loss. Pain around the eye occurs, especially with movement of the globe. This may occur with visual field defects and a sluggish pupillary response to light. Ophthalmoscopic examination commonly reveals hyperemia of the optic disk, blurred disk margins, and filling of the physiologic cup.
With Paget’s disease, bilateral vision loss may develop as a result of bony impingements on the cranial nerves. This occurs with hearing loss, tinnitus, vertigo, and severe, persistent bone pain. Cranial enlargement may be noticeable frontally and occipitally, and headaches may occur. Sites of bone involvement are warm and tender, and impaired mobility and pathologic fractures are common.
Papilledema is characterized by swelling of the optic disk from increased intracranial pressure; both optic disks are affected. Acute papilledema may lead to momentary blurring or transiently obscured vision, whereas chimeric papilledema may lead to vision loss.
As a pituitary adenoma grows, blurred vision progresses to hemianopia and, possibly, unilateral blindness. Double vision, nystagmus, ptosis, limited eye movement, and headaches may also occur.
Retinal artery occlusion is a painless ocular emergency that causes sudden unilateral vision loss, which may be partial or complete. Pupil examination reveals a sluggish direct pupillary response and a normal consensual response. Permanent blindness may occur within hours.
Depending on the degree and location of retinal detachment, painless vision loss may be gradual or sudden and total or partial. Macular involvement causes total blindness.
With partial vision loss, the patient may describe visual field defects or a shadow or curtain over the visual field as well as visual floaters.
Most common in geriatric patients, retinal vein occlusion is a painless disorder that causes a unilateral decrease in visual acuity with variable vision loss. IOP may be elevated in both eyes.
Occurring in elderly patients, senile macular degeneration causes painless blurring or loss of central vision. Vision loss may proceed slowly or rapidly, eventually affecting both eyes. Visual acuity may be worse at night.
Vision loss and visual blurring with a throbbing, unilateral headache characterize temporal arteritis. Other findings include malaise, anorexia, weight loss, weakness, low-grade fever, generalized muscle aches, and confusion.
Inflammation of the uveal tract may result in unilateral vision loss. Anterior uveitis produces moderate to severe eye pain, severe conjunctival injection, photophobia, and a small, nonreactive pupil. Posterior uveitis may produce insidious onset of blurred vision, conjunctival injection, visual floaters, pain, and photophobia. Associated posterior scar formation distorts the shape of the pupil.
With vitreous hemorrhage, sudden unilateral vision loss may result from intraocular trauma, ocular tumors, or systemic disease (especially diabetes, hypertension, sickle cell anemia, or leukemia). Visual floaters and partial vision with a reddish haze may occur. The patient’s vision loss may be permanent.
Chloroquine therapy may cause patchy retinal pigmentation that typically leads to blindness. Phenylbutazone may cause vision loss and increased susceptibility to retinal detachment. Cardiac glycoside derivatives, indomethacin, ethambutol, quinine sulfate, and methanol toxicity may also cause vision loss.
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Amaurosis fugax.With amaurosis fugax, recurrent attacks of unilateral vision loss may last from a few seconds to a few minutes. Vision is normal at other times. Transient unilateral weakness, hypertension, and elevated intraocular pressure (IOP) in the affected eye may also occur.
Cataract.With a cataract, painless and gradual visual blurring typically precede vision loss. As the cataract progresses, the pupil turns milky white.
Concussion.Immediately or shortly after blunt head trauma, vision may be blurred, double, or lost. Generally, vision loss is temporary. Other findings include headache, anterograde and retrograde amnesia, transient loss of consciousness, nausea, vomiting, dizziness, irritability, confusion, lethargy, and aphasia.
Diabetic retinopathy.With diabetic retinopathy, retinal edema and hemorrhage lead to visual blurring, which may progress to blindness.
Endophthalmitis.Typically, endophthalmitis follows penetrating trauma, I.V. drug use, or intraocular surgery, causing possibly permanent unilateral vision loss; a sympathetic inflammation may affect the other eye.
Glaucoma.Glaucoma produces gradual visual blurring that may progress to total blindness. Acute angle-closure glaucoma is an ocular emergency that may produce blindness within 3 to 5 days. Findings are rapid onset of unilateral inflammation and pain, pressure over the eye, moderate pupil dilation, nonreactive pupillary response, a cloudy cornea, reduced visual acuity, photophobia, and perception of blue or red halos around lights. Nausea and vomiting may also occur.
Chronic angle-closure glaucoma has a gradual onset and usually produces no symptoms, although blurred or halo vision may occur. If untreated, it progresses to blindness and extreme pain.
Chronic open-angle glaucoma is usually bilateral, with an insidious onset and a slowly progressive course. It causes peripheral vision loss, aching eyes, halo vision, and reduced visual acuity (especially at night).
Ocular trauma.Following eye injury, sudden unilateral or bilateral vision loss may occur. Vision loss may be total or partial and permanent or temporary. The eyelids may be reddened, edematous, and lacerated; intraocular contents may be extruded.
Optic atrophy.Optic atrophy can develop spontaneously or follow inflammation or edema of the nerve head, causing irreversible loss of the visual field with changes in color vision. Pupillary reactions are sluggish and optic disk pallor is evident.
Optic neuritis.An umbrella term for inflammation, degeneration, or demyelinization of the optic nerve, optic neuritis usually produces temporary but severe unilateral vision loss. Pain around the eye occurs, especially with movement of the globe. This may occur with visual field defects and a sluggish pupillary response to light. Ophthalmoscopic examination commonly reveals hyperemia of the optic disk, blurred disk margins, and filling of the physiologic cup.
Paget's disease.With Paget's disease, bilateral vision loss may develop as a result of bony impingements on the cranial nerves. This occurs with hearing loss, tinnitus, vertigo, and severe, persistent bone pain. Cranial enlargement may be noticeable frontally and occipitally, and headaches may occur. Sites of bone involvement are warm and tender and impaired mobility and pathologic fractures are common.
Pituitary tumor.As a pituitary adenoma grows, blurred vision progresses to hemianopsia and, possibly, unilateral blindness. Double vision, nystagmus, ptosis, limited eye movement, and headaches may also occur.
Retinal artery occlusion (central).Retinal artery occlusion is a painless ocular emergency that causes sudden unilateral vision loss, which may be partial or complete. Pupil examination reveals a sluggish direct pupillary response and a normal consensual response. Permanent blindness may occur within hours.
Retinal detachment.Depending on the degree and location of retinal detachment, painless vision loss may be gradual or sudden and total or partial. Macular involvement causes total blindness.
With partial vision loss, the patient may describe visual field defects or a shadow or curtain over the visual field as well as visual floaters.
Retinal vein occlusion (central).Retinal vein occlusion causes a unilateral decrease in visual acuity with variable vision loss. IOP may be elevated in both eyes.
Rift Valley fever.Rift Valley fevercauses inflammation of the retina and may result in some permanent vision loss. Typical signs and symptoms include fever, myalgia, weakness, dizziness, and back pain. A small percentage of patients may develop encephalitis or may progress to hemorrhagic fever that can lead to shock and hemorrhage.
Senile macular degeneration.Senile macular degeneration causes painless blurring or loss of central vision. Vision loss may proceed slowly or rapidly, eventually affecting both eyes. Visual acuity may be worse at night.
Stevens-Johnson syndrome.With Stevens-Johnson syndrome, corneal scarring from associated conjunctival lesions produces marked vision loss. Purulent conjunctivitis, eye pain, and difficulty opening the eyes occur. Additional findings include widespread bullae, fever, malaise, cough, drooling, inability to eat, sore throat, chest pain, vomiting, diarrhea, myalgias, arthralgias, hematuria, and signs of renal failure.
Temporal arteritis.Vision loss and visual blurring with a throbbing, unilateral headache characterize temporal arteritis. Other findings include malaise, anorexia, weight loss, weakness, low-grade fever, generalized muscle aches, and confusion.
Vitreous hemorrhage.With vitreous hemorrhage, sudden unilateral vision loss may result from intraocular trauma, ocular tumors, or systemic disease (especially diabetes, hypertension, sickle cell anemia, or leukemia). Visual floaters and partial vision with a reddish haze may occur. The patient's vision loss may be permanent.
Drugs.Chloroquine therapy may cause patchy retinal pigmentation that typically leads to blindness. Phenylbutazone may cause vision loss and increased susceptibility to retinal detachment. Digoxin, indomethacin, ethambutol, quinine sulfate, and methanol toxicity may also cause vision loss.
Source: Nursing: Interpreting Signs and Symptoms, 2007
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