Vascular disorders that affect the eyes include central retinal artery occlusion, central retinal vein occlusion, ischemic optic neuropathy, amaurosis fugax, and occipital lobe vascular accident.

CENTRAL RETINAL ARTERY OCCLUSION
Occlusion of the central retinal artery produces sudden blindness in the affected eye. The typical cause in older patients is an atheroma, usually broken off the carotid artery wall. The atheroma occludes the central retinal artery in the deeper portion of the optic nerve head and thus cannot be seen. Within an hour after loss of vision, the arterial spasm ceases, and some blood flow is restored to the retina, giving the appearance of a relatively normal retina on ophthalmoscopy. However, within several hours, the retina becomes edematous and gray from the death of retinal ganglion cells. Because the retina in the foveal area contains no ganglion cells, the reddish underlying choroid remains visible, accounting for the characteristic central cherry-red spot surrounded by gray retina. In 2 to 3 wk, the cherry-red spot disappears, and as the ganglion cells and their axons die, the optic nerve becomes white, the hallmark of primary optic atrophy.
When an atheroma breaks off, passes through the central retinal artery, and lodges in a retinal artery branch, it can usually be seen as a retractile object in the branch and is referred to as a Hollenhorst plaque. This finding indicates embolic activity, usually from the carotid system. The portion of the retina supplied by the occluded vessel loses its function and a visual field defect, which may not affect central vision, results.
Intervention is needed within a few minutes of the occlusion to prevent retinal cell death. Acutely reducing intraocular pressure by paracentesis combined with vasodilators may occasionally prevent this complication.
CENTRAL RETINAL VEIN OCCLUSION
Retinal vein occlusion is probably the most common vascular accident in the eye. About 10% of patients having a central retinal vein occlusion in one eye will also develop one in the other eye. Even after the occlusion occurs, some vision remains.
Ophthalmoscopy reveals distended, tortuous veins with massive hemorrhages and edema throughout the retina. The margins of the optic nerve become blurred and the disk swollen. Complete resorption of the hemorrhages and edema may take months or even years. In the older patient, the prognosis for vision is poor. Also, about 25% of patients develop a fibrovascular membrane that seals the aqueous humor outflow channels in the anterior chamber, resulting in a painful neovascular glaucoma in 3 to 6 mo. If the intraocular pressure remains elevated, blindness results in weeks. Treatment is most often attempted with laser photocoagulation, but its effectiveness is still being assessed.
Branch vein occlusion is also seen when a branch of the central retinal vein becomes obstructed, most often the superior temporal branch. The characteristic exudates and hemorrhages are confined to the involved quadrant of the retina, which has an associated visual field defect. Vision is usually unaffected unless the retinal swelling impinges on the macula. A clinical trial has demonstrated that using laser photocoagulation to treat branch vein occlusion helps preserve vision. Fortunately, the development of neovascular glaucoma is much less common in branch vein occlusion.

Occlusion of the central retinal artery produces sudden blindness in the affected eye. The typical cause in older patients is an atheroma, usually broken off the carotid artery wall. The atheroma occludes the central retinal artery in the deeper portion of the optic nerve head and thus cannot be seen. Within an hour after loss of vision, the arterial spasm ceases, and some blood flow is restored to the retina, giving the appearance of a relatively normal retina on ophthalmoscopy. However, within several hours, the retina becomes edematous and gray from the death of retinal ganglion cells. Because the retina in the foveal area contains no ganglion cells, the reddish underlying choroid remains visible, accounting for the characteristic central cherry-red spot surrounded by gray retina. In 2 to 3 wk, the cherry-red spot disappears, and as the ganglion cells and their axons die, the optic nerve becomes white, the hallmark of primary optic atrophy.
When an atheroma breaks off, passes through the central retinal artery, and lodges in a retinal artery branch, it can usually be seen as a retractile object in the branch and is referred to as a Hollenhorst plaque. This finding indicates embolic activity, usually from the carotid system. The portion of the retina supplied by the occluded vessel loses its function and a visual field defect, which may not affect central vision, results.
Intervention is needed within a few minutes of the occlusion to prevent retinal cell death. Acutely reducing intraocular pressure by paracentesis combined with vasodilators may occasionally prevent this complication.

Retinal vein occlusion is probably the most common vascular accident in the eye. About 10% of patients having a central retinal vein occlusion in one eye will also develop one in the other eye. Even after the occlusion occurs, some vision remains.
Ophthalmoscopy reveals distended, tortuous veins with massive hemorrhages and edema throughout the retina. The margins of the optic nerve become blurred and the disk swollen. Complete resorption of the hemorrhages and edema may take months or even years. In the older patient, the prognosis for vision is poor. Also, about 25% of patients develop a fibrovascular membrane that seals the aqueous humor outflow channels in the anterior chamber, resulting in a painful neovascular glaucoma in 3 to 6 mo. If the intraocular pressure remains elevated, blindness results in weeks. Treatment is most often attempted with laser photocoagulation, but its effectiveness is still being assessed.
Branch vein occlusion is also seen when a branch of the central retinal vein becomes obstructed, most often the superior temporal branch. The characteristic exudates and hemorrhages are confined to the involved quadrant of the retina, which has an associated visual field defect. Vision is usually unaffected unless the retinal swelling impinges on the macula. A clinical trial has demonstrated that using laser photocoagulation to treat branch vein occlusion helps preserve vision. Fortunately, the development of neovascular glaucoma is much less common in branch vein occlusion.

Regardless of the cause, ischemic optic neuropathy almost always occurs in those > 60 yr. Partial or complete loss of vision occurs suddenly, accompanied by swelling of the optic nerve head and often a hemorrhage or two. A visual field defect may produce a loss of half the visual field with a horizontal demarcation. Ischemic optic neuropathy is a medical emergency.
When temporal arteritis is the cause, tenderness along the temporal artery may be noted, as well as headache, jaw pain while chewing, and fever. Symptoms are almost always accompanied by an elevated erythrocyte sedimentation rate. Generally, prednisone 60 mg/day should be started as soon as possible, and a temporal artery biopsy should be obtained.
When atheromatosis is the cause of ischemic optic neuropathy, pain is uncommon, and decreased vision is soon followed by pallor of the optic disk. The visual loss in the other eye may occur months or years later, and once the ischemic episode has occurred, treatment does not help. In selected older patients with a history of blackouts (amaurosis fugax) suggestive of atheromatosis, long-term anticoagulant therapy may help.

AMAUROS?S FUGAX(Blackouts)
When unilateral, amaurosis fugax suggests either retinal or optic nerve ischemia. The blackout may present as a dimming of vision with a slow recovery beginning after 5 to 10 min. The restoration of clear vision occurs in the reverse order from the onset pattern. Several episodes of blackout may precede an attack of ischemic optic neuropathy, or episodes may occur for years without serious sequelae. However, patients experiencing such episodes should be under medical care. The blackout can be bilateral if associated with low blood pressure.
Unilateral blackouts are characteristic of carotid artery narrowing,
usually at the bifurcation of the common carotid artery. Because ather
oma is the major cause of vessel narrowing, patients > 50 yr are most
susceptible. Obstruction of the left carotid artery is six times more com
mon than that of the right.    f
When blackout is accompanied by hemiplegia on the side opposite the affected eye (transient ischemic attack), carotid stenosis on the side of the affected eye should be strongly suspected. Early recognition of serious carotid stenosis is important because many affected patients will develop permanent visual loss or hemiplegia without appropriate medical and surgical intervention.

The aortic arch syndrome may be suspected if increasingly frequent blackouts are related to changes in posture, such as suddenly sitting up or standing.

A vascular lesion of the occipital lobe, usually the result of a posterior cerebral artery infarction, is usually characterized by sudden homonymous hemianopia. Infarction in one or both occipital lobes may result from local atheromatous disease, vascular insufficiency, or emboli in the vertebral-basilar system. Total blindness occurs suddenly, with some vision returning within minutes in the ipsilateral homonymous visual field. Bilateral posterior occlusions usually occur simultaneously. Thrombosis of the basilar artery also produces a bilateral homonymous hemianopia. In almost all cases of cortical blindness, some vision returns.

Miscellaneous conditions affecting the elderly include acute double vision, diabetic ophthalmoplegia, intracranial tumor, and myasthenia gravis.
ACUTE DOUBLE VISION
The third cranial nerve innervates the medial, superior, and inferior rectus muscles, the inferior oblique muscle, and the levator muscle and also carries the parasympathetic nerves ponstricting the pupil and controlling accommodation. A complete third cranial nerve palsy results in ptosis; a divergence of the eye when looking straight ahead; a dilated fixed pupil; and a lack of upward, inward, and downward eye movement. The main causes of isolated third cranial nerve palsy are intracranial aneurysm, trauma, and diabetic neuropathy. Palsy from diabetes mellitus clears spontaneously in 6 to 12 wk, but palsy from intracranial aneurysm or trauma requires immediate diagnostic and, if indicated, therapeutic intervention.
The fourth cranial nerve innervates the superior oblique muscle, and palsy invariably results from a small hemorrhage in the roof of the midbrain, usually from arteriosclerosis. Recovery occurs spontaneously after several weeks.
The sixth cranial nerve innervates the lateral rectus muscle and, because it has the longest intracranial course, is often affected by meningitis, skull fracture, and increased intracranial pressure. When the nerve is affected by diabetes mellitus, spontaneous recovery occurs in 6 to 12 wk.
DIABETIC OPHTHALMOPLEGIA
Severe eye or forehead pain followed by a third cranial nerve palsy that spares the pupil should be considered a manifestation of diabetic neuropathy.
INTRACRAN?AL TUMOR
An intracranial space-occupying mass is often accompanied by increased intracranial pressure and severe headache. Ophthalmoscopy may show papilledema. Prompt referral for a neurosurgical diagnostic evaluation is indicated.
MYASTHEN?A GRAV?S
Any combination of extraocular muscle palsies, which may vary in severity over days or weeks, along with a normal pupillary response to light and a history of fatigue that waxes and wanes during the day should raise the possibility of myasthenia gravis. An edrophonium chloride (Tensilon) test should help establish the diagnosis.

The third cranial nerve innervates the medial, superior, and inferior rectus muscles, the inferior oblique muscle, and the levator muscle and also carries the parasympathetic nerves ponstricting the pupil and controlling accommodation. A complete third cranial nerve palsy results in ptosis; a divergence of the eye when looking straight ahead; a dilated fixed pupil; and a lack of upward, inward, and downward eye movement. The main causes of isolated third cranial nerve palsy are intracranial aneurysm, trauma, and diabetic neuropathy. Palsy from diabetes mellitus clears spontaneously in 6 to 12 wk, but palsy from intracranial aneurysm or trauma requires immediate diagnostic and, if indicated, therapeutic intervention.
The fourth cranial nerve innervates the superior oblique muscle, and palsy invariably results from a small hemorrhage in the roof of the midbrain, usually from arteriosclerosis. Recovery occurs spontaneously after several weeks.
The sixth cranial nerve innervates the lateral rectus muscle and, because it has the longest intracranial course, is often affected by meningitis, skull fracture, and increased intracranial pressure. When the nerve is affected by diabetes mellitus, spontaneous recovery occurs in 6 to 12 wk.

Severe eye or forehead pain followed by a third cranial nerve palsy that spares the pupil should be considered a manifestation of diabetic neuropathy.

An intracranial space-occupying mass is often accompanied by increased intracranial pressure and severe headache. Ophthalmoscopy may show papilledema. Prompt referral for a neurosurgical diagnostic evaluation is indicated.