Acute Visual Loss and Double Vision

Approach to the patient

Accurate measurement of visual acuity in each eye (with glasses or contact lenses) 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 examination to inspect the optic disc and retina often requires pupillary dilation using 1% tropicamide 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. 52-1); formal testing using a perimeter may be necessary. The goal is to determine whether the lesion is anterior to, 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 examination 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.


Deficits in visual fields caused by lesions affecting visual pathways.


Amaurosis fugax (transient monocular blindness; a TIA of the retina) usually occurs from a retinal embolus often arising from ipsilateral carotid stenosis or the heart. 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 atheroma, heart disease, atrial fibrillation). Occipital cortex lesions 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, especially those of posterior circulation dysfunction such as diplopia, vertigo, numbness, or weakness.

Marked systemic 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 examination reveals engorged, phlebitic veins with extensive retinal hemorrhages.

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 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. Enlarged blind spots and peripheral constriction are typical. Neuroimaging should be obtained to exclude an intracranial mass. If negative, a 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 (via bariatric surgery if necessary); some pts require lumboperitoneal shunting to prevent blindness.

Optic neuritis is a common cause of monocular optic disc swelling and visual loss. If site of inflammation is retrobulbar, fundus will appear normal on initial examination. The typical pt is female, age 15–45, with pain provoked by eye movements. Glucocorticoids, typically IV methylprednisolone (1 g daily for 3 days) followed by oral prednisone (1 mg/kg daily for 11 days), may hasten recovery in severely affected pts but make no difference in final acuity (measured 6 months after the attack). If an MRI shows multiple demyelinating lesions, treatment for multiple sclerosis (Chap. 190) should be considered. Optic neuritis involving both eyes simultaneously or sequentially suggests neuromyelitis optica.

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 noted on awakening, and painless swelling of the optic disc. It is important to differentiate between nonarteritic (idiopathic) AION and arteritic AION. There is no treatment for nonarteritic AION. In contrast, arteritic AION is caused by giant cell (temporal) arteritis and requires immediate glucocorticoid therapy to prevent blindness; temporal artery biopsy establishes the diagnosis. The ESR and C-reactive protein should be checked in any elderly pt with acute optic disc swelling or symptoms suggestive of polymyalgia rheumatica (associated with arteritic AION).


First step: clarify whether diplopia persists in either eye after covering the opposite eye; if it does the diagnosis is monocular diplopia usually caused by disease intrinsic to the eye with no dire implications for the pt. Occasionally it is a symptom of malingering or psychiatric disease.

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

Common causes of diplopia are summarized in Table 52-1. The physical findings in isolated ocular motor nerve palsies are:

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
Myasthenia gravis
Guillain-Barré or Fisher syndrome
Graves’ disease
Orbital pseudotumor
Orbital myositis
Orbital cellulitis
  • CN III: Ptosis and deviation of the eye down and outwards, causing vertical and horizontal diplopia. A dilated pupil suggests direct compression of the third nerve; if present, the possibility of an aneurysm of the posterior communicating artery must be considered urgently. If pupil is spared, a microvascular infarction is likely the cause, especially in pts with diabetes or hypertension.
  • 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 worse on gaze to the side of the lesion; the affected eye cannot abduct.

The development 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. Multiple ocular motor nerve palsies should be investigated with neuroimaging focusing on the cavernous sinus, superior orbital fissure, and orbital apex where all three nerves are in close proximity. Diplopia that cannot be explained by a single ocular motor nerve palsy may also be caused by carcinomatous or fungal meningitis, Graves’ disease, Guillain-Barré syndrome (especially the Miller Fisher variant), or Tolosa-Hunt syndrome (painful granulomatous inflammation of the cavernous sinus).

For a more detailed discussion

For a more detailed discussion, see Horton JC: Disorders of the Eye, Chap. 39, p. 195, in HPIM-19.

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