Acute Visual Loss and Double Vision

Clinical Assessment

Accurate measurement of visual acuity in each eye (with glasses) is of primary

importance. Additional assessments include testing of pupils,eye movements,

ocular alignment,and visual fields. Slit-lamp examination can exclude corneal

infection,trauma, glaucoma,uveitis, and cataract. Ophthalmoscopic exam to

inspect the optic disc and retina often requires pupillary dilation using 1% topicamide

and 2.5% phenylephrine; risk of provoking an attack of narrow-angle

glaucoma is remote.

Visual field mapping by finger confrontation localizes lesions in the visual

pathway (Fig. 40-1); formal testing using a perimeter may be necessary. The

goal is to determine whether the lesion is anterior,at,or posterior to the optic

chiasm. A scotoma confined to one eye is caused by an anterior lesion affecting

the optic nerve or globe; swinging flashlight test may reveal an afferent pupil

defect. History and ocular exam are usually sufficient for diagnosis. If a bitemporal

hemianopia is present,lesion is located at optic chiasm (e.g., pituitary

adenoma,meningioma). Homonymous visual field loss signals a retrochiasmal

lesion, affecting the optic tract,lateral geniculate body,optic radiations, or visual cortex (e.g.,stroke,tumor, abscess). Neuroimaging is recommended for

any pt with a bitemporal or homonymous hemianopia.

Transient or Sudden Visual Loss

Amaurosis fugax (transient monocular blindness) usually occurs from a retinal

embolus or severe ipsilateral carotid stenosis. Prolonged occlusion of the central

retinal artery results in classic fundus appearance of a milky,infarcted retina

with cherry-red fovea. Any pt with compromise of the retinal circulation should

be evaluated promptly for stroke risk factors (e.g.,carotid atheromata, heart

disease,atrial fibrillation).

Vertebrobasilar insufficiency or emboli can be confused with amaurosis

fugax,because many pts mistakenly ascribe symptoms to their left or right eye,

when in fact they are occurring in the left or right hemifield of both eyes.

Interruption of blood flow to the visual cortex causes sudden graying of vision,

occasionally with flashing lights or other symptoms that mimic migraine. The

history may be the only guide to the correct diagnosis. Pts should be questioned

about the precise pattern and duration of visual loss and other neurologic symptoms such as diplopia,vertigo,numbness, or weakness, which may help decide

between compromise of the anterior or posterior cerebral circulation.

Malignant hypertension can cause visual loss from exudates,hemorrhages,

cotton-wool spots (focal nerve fiber layer infarcts),and optic disc edema. In

central or branch retinal vein occlusion,the fundus exam reveals engorged,

dusky veins with extensive retinal bleeding. In age-related macular degeneration,

characterized by extensive drusen and scarring of the pigment epithelium,

leakage of blood or fluid from subretinal neovascular membranes can produce

sudden central visual loss. Flashing lights and floaters may indicate a fresh

vitreous detachment. Separation of the vitreous from the retina is a frequent

involutional event in the elderly. It is not harmful unless it creates sufficient

traction to produce a retinal detachment. Vitreous hemorrhage may occur in

diabetic pts from retinal neovascularization.

Papilledema refers to bilateral optic disc edema from raised intracranial

pressure. Transient visual obscurations are common,but visual acuity is not

affected unless the papilledema is severe,long-standing,or accompanied by

macular exudates or hemorrhage. Neuroimaging should be obtained to exclude

an intracranial mass. If negative,an LP is required to confirm elevation of the

intracranial pressure. Pseudotumor cerebri (idiopathic intracranial hypertension)

is a diagnosis of exclusion. Most pts are young,female, and obese; some

are found to have occult cerebral venous sinus thrombosis. Treatment is with

acetazolamide,repeated LPs, and weight loss; some pts require lumboperitoneal

shunting or optic nerve sheath fenestration. Optic neuritis is a common cause

of monocular optic disc swelling and visual loss,although it rarely affects both

eyes. If site of inflammation is retrobulbar,fundus will appear normal on initial

exam. The typical pt is female,age 15–45,with pain provoked by eye movements.

Glucocorticoids,consisting of intravenous methylprednisolone (1 g daily

for 3 days) followed by oral prednisone (1 mg/kg daily for 11 days),may hasten

recovery in severely affected patients. If an MR scan shows multiple demyelinating lesions,treatment for multiple sclerosis should be considered. Anterior ischemic optic neuropathy (AION) is an infarction of the optic nerve head due to inadequate perfusion via the posterior ciliary arteries. Pts have sudden visual

loss,often upon awakening,and painless swelling of the optic disc. It is important

to differentiate between nonarteritic (idiopathic) AION and arteritic

AION. The latter is caused by temporal arteritis and requires immediate glucocorticoid therapy. The ESR should be checked in any elderly pt with acute

optic disc swelling or symptoms suggestive of polymyalgia rheumatica.

Double Vision (Diplopia)

If pt has diplopia while being examined,motility testing will usually reveal

abnormality in ocular excursions. However,if the degree of angular separation

between the double images is small,the limitation of eye movements may be

subtle and difficult to detect. In this situation,the cover test is useful. While the

pt is fixating upon a distant target,one eye is covered while observing the other

eye for a movement of redress as it takes up fixation. If none is seen,the

procedure is repeated with the other eye. With genuine diplopia,this test should

reveal ocular malalignment,especially if the head is turned or tilted in the

position that gives rise to the worst symptoms.

The most frequent causes of diplopia are summarized in Table 40-1. The

physical findings in isolated ocular motor nerve palsies are:

• CN III: Ptosis and deviation of the eye down and outwards,causing vertical

and horizontal diplopia. Pupil dilation suggests direct compression of the third

nerve; if present,the possibility of an aneurysm of the posterior communicating

artery must be considered urgently.

• CN IV: Vertical diplopia with cyclotorsion; the affected eye is slightly elevated,

and limitation of depression is seen when the eye is held in adduction.

The pt may assume a head tilt to the opposite side (e.g.,left head tilt in right

fourth nerve paresis).

• CN VI: Horizontal diplopia with crossed eyes; the affected eye cannot abduct.

Isolated ocular motor nerve palsies often occur in pts with hypertension or

diabetes. They usually resolve spontaneously over several months. The apparent

occurrence of multiple ocular motor nerve palsies,or diffuse ophthalmoplegia,

raises the possibility of myasthenia gravis. In this disease,the pupils are always

normal. Systemic weakness may be absent. Diplopia that cannot be explained

by a single ocular motor nerve palsy may also be caused by carcinomatous or fungal meningitis,Graves’ disease, Guillain-Barre´ syndrome,Fisher’s syndrome,

or Tolosa-Hunt syndrome.

Common Causes of Diplopia

Brainstem stroke (skew deviation,nuclear or fascicular palsy)

Microvascular infarction (III,IV, VI nerve palsy)

Tumor (brainstem,cavernous sinus, superior orbital fissure, orbit)

Multiple sclerosis (internuclear ophthalmoplegia,ocular motor nerve palsy)

Aneurysm (III nerve)

Raised intracranial pressure (VI nerve)

Postviral inflammation

Meningitis (bacterial,fungal, granulomatosis, neoplastic)

Carotid-cavernous fistula or thrombosis

Herpes zoster

Tolosa-Hunt syndrome

Wernicke-Korsakoff syndrome

Botulism

Myasthenia gravis

Guillain-Barre´ or Fisher syndrome

Graves’ disease

Orbital pseudotumor

Orbital myositis

Trauma

Orbital cellulitis