Double vision or diplopia is defined simply as seeing one object as two and may be monocular or binocular. The sudden onset of diplopia is a dramatic event and therefore a cause for great anxiety and concern. For this reason and because of the serious nature of many of the causes of diplopia, meticulous attention must be paid to the neuro-ophthalmologic examination.

Distinguishing monocular diplopia from binocular diplopia is an important initial consideration in the evaluation of patients with double vision. Monocular diplopia is usually psychogenic in origin but rarely may be associated with subluxation of the lens, cataracts, macular lesions or edema, or detachment of the retina. Each of these may be detected by a careful ophthalmologic examination. Binocular diplopia is more common than monocular diplopia and is generally caused by three general classes of disorders: metabolic, extraocular muscle, or local periorbital abnormalities.

Dysarthria, somnolence, incoordination, and the odor of alcohol on the breath all suggest recent alcohol ingestion as a cause for diplopia. Nystagmus, extraocular palsy, lower limb ataxia, and, in severe cases, coma suggest acute Wernicke encephalopathy (thiamine deficiency). An isolated sixth nerve palsy is most commonly found in diabetic neuropathy; however, the third, fourth, and fifth cranial nerves may also be involved in an asymmetric, mononeuritis multiplex pattern. In patients with diabetic neuropathy, the pupillary fibers of the third cranial nerve are “spared” pathologic change, and the pupil reacts normally to light. In contrast, in patients with mass lesions (including cerebral aneurysms) compressing the third cranial nerve externally, pupillary dilation and a sluggish or absent light response are the rule. Periorbital ecchymosis (“raccoon eyes”) or edema suggests trauma-related extraocular muscle entrapment or cranial nerve contusion. Cerebrovascular accidents associated with diplopia often involve brainstem structures and findings involving other cranial nerves or the pyramidal tracts (or both) should be sought in patients in whom a stroke is suspected (i.e., patients with atrial fibrillation or elderly persons with hypertension). Weakness of the periorbital musculature, dysphonia, neck flexion weakness, and increasing weakness on repetitive muscle stimulation (i.e., repeated hand grip) are all suggestive of myasthenia gravis. Anatomically and temporally disparate associated neurologic deficits characterize multiple sclerosis. Neck stiffness accompanying headache and diplopia may be seen in patients with meningitis or intracranial aneurysm or hemorrhage.

A blood alcohol level may be elevated in persons manifesting acute alcoholic toxicity. In patients with acute Wernicke encephalopathy, alcohol need not be detected in the blood, nor do patients necessarily manifest signs of alcohol toxicity. The administration of thiamine, 100 to 500 mg intravenous, serves as both a therapeutic and diagnostic maneuver in that patients with acute Wernicke encephalopathy will respond with an improvement in muscle function and a disappearance of diplopia. A random blood glucose or, if not elevated, an oral glucose tolerance test will help diagnose
diabetics with neuropathy. Orbital and facial roentgenograms or computed tomography (CT) scanning are mandatory for the diagnosis of suspected orbital or facial fractures. An emergency CT scan of the head and possibly lumbar puncture are indicated in patients with diplopia and either a severe headache or abnormalities of mental status.

Although emergency physicians are most commonly confronted with abnormalities of extraocular muscle function caused by cranial nerve palsies, a number of other conditions affecting extraocular motor function should be noted.