Diplopia
Zoe Williams
Jonathan Strong
THE CLINICAL CHALLENGE
Diplopia—colloquially referred to as “double vision”—is a challenging chief complaint in the emergency and urgent care setting. It is also an infrequent chief complaint in the emergency and urgent care setting, representing 0.1% of all ED visits.1 Diplopia may occur from a wide spectrum of pathologies including many benign causes (e.g. decompensated phoria, convergence or divergence insufficiency, and microvascular disease) as well as vision- or lifethreatening causes (e.g. stroke, cerebral aneurysm, brain tumor, intracranial hemorrhage, thyroid eye disease, giant cell arteritis, myasthenia gravis, meningitis, cavernous sinus thrombosis, or increased intracranial pressure). Structural lesions causing diplopia may localize to the cortical, subcortex, brainstem, subarachnoid, cavernous sinus or orbital level. A comprehensive review of all causes of diplopia is beyond the scope of this chapter, but several important causes to consider in the emergency and urgent care settings are listed in Table 49-1.
The clinician should first determine whether the diplopia is monocular or binocular. Monocular diplopia is confirmed when covering the unaffected eye does not resolve the diplopia. This strongly suggests a single eye problem such as dry eye, refractive error, corneal pathology, cataract, or retinal disease. These patients warrant a thorough eye exam, but monocular diplopia is generally not an emergency.
In contrast, binocular diplopia resolves with occlusion of either eye indicating misalignment of the visual axes. This chapter describes the evaluation of binocular diplopia (henceforth referred to as diplopia) with an emphasis on identifying emergent disease entities that clinicians must consider.
PATHOPHYSIOLOGY
A brief review of the neuroanatomy of eye movement is helpful to recognize patterns of extraocular muscle weakness, identify cranial nerve (CN) palsies, and localize structural lesions. The eye moves in three axes: horizontal (adduction and abduction), vertical (supraduction and infraduction), and torsional (intorsion and extorsion).
CN III (oculomotor nerve) originates from the dorsal midbrain and innervates four of the six extraocular muscles: the medial rectus, inferior rectus, inferior oblique muscles (inferior division), and superior rectus (superior division). Motor fibers of the superior division also innervate the levator muscle of the eyelid. In addition, CN III contains parasympathetic fibers on the periphery that control pupil constriction, making them susceptible to compressive lesions. Patients with a complete CN III palsy present with ptosis and the inability to supraduct, infraduct, or adduct the eye. As a result, the affected eye will display exotropia and hypotropia (the “down and out” position) (Figure 49.1). An incomplete CN III palsy will present with varying degrees of weakness in each of the extraocular muscles and/or levator palpebrae. It is important to note that complete and incomplete refer only to the motor function of CN III. The parasympathetic fibers act independently, and thus patients with complete or incomplete CN III palsy may or may not have pupil involvement.
CN IV (trochlear nerve) possesses the longest intracranial length, making it particularly susceptible to injury. It originates from the dorsal midbrain and ultimately innervates a single extraocular muscle, the superior oblique. A patient with CN IV palsy may display hypertropia and excyclotorsion in the affected eye; however, these deficits are often not readily apparent on gross examination owing to the compensatory effect of other extraocular muscles (Figure 49.2). To diagnose an isolated unilateral CN IV palsy, the examiner should assess whether the hypertropia in the affected eye worsens with gaze toward the contralateral side and with head tilt toward the ipsilateral side (the Parks-Bielschowsky method). One should note, however, that the sensitivity
and specificity of this combination of findings is limited.2,3,4 If the hypertropia does not follow this characteristic pattern, one should consider alternative causes.
and specificity of this combination of findings is limited.2,3,4 If the hypertropia does not follow this characteristic pattern, one should consider alternative causes.
TABLE 49.1 Selected Causes of Diplopia | ||||||||||||
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 Figure 49.1: Left oculomotor (CN III) nerve palsy. (From Agur AM, Dalley AF. Moore’s Essential Clinical Anatomy. 6th ed. Wolters Kluwer; 2020. UnFigure 8.11.) |
 Figure 49.2: Trochlear nerve palsy of the left eye. (Images courtesy of Jason Peragallo, MD. In: Sherman SC, Ross C, Nordquist E, Wang E, Cico S, eds. Atlas of Clinical Emergency Medicine. 1st ed. Wolters Kluwer; 2016. Figure 2.19.) |
CN VI (abducens nerve) originates from the pons and ultimately innervates the lateral rectus muscle. A patient with an isolated unilateral CN VI palsy will display esotropia most apparent on ipsilateral gaze and/or inability to abduct the affected eye fully (Figure 49.3). Elevated intracranial pressure caused by structural lesions or idiopathic intracranial hypertension may cause traction on CN VI as it travels along the clivus, resulting in unilateral or bilateral CN VI palsy.
Diplopia in the setting of head trauma may be caused by decompensated phoria, convergence insufficiency, CN palsies (CN III, IV, VI paresis) attributable to stretch injury, hemorrhage of a preexisting brain lesion with resultant compressive injury, intracranial hemorrhage, direct extraocular muscle damage, extraocular muscle entrapment attributable to orbital fracture, orbital compartment syndrome secondary to retrobulbar hematoma, or a direct carotid-cavernous fistula. Usually direct carotid-cavernous fistulas will present with other ocular signs such as arterialization of the conjunctival vessels, chemosis, proptosis, and elevated intraocular pressure in addition to diplopia; however, diplopia is occasionally the only finding. Thus, patients should be asked if they have an audible bruit suggestive of a carotid-cavernous fistula.
 Figure 49.3: Left CNVI (abducens nerve) palsy. (Images courtesy of Jason Peragallo, MD. In: Sherman SC, Ross C, Nordquist E, Wang E, Cico S, eds. Atlas of Clinical Emergency Medicine. 1st ed. Wolters Kluwer; 2016. Figure 2.1.) |
Patients with a history of malignancy, including skin cancer, particularly those with progressive facial numbness, paresthesias, or weakness, should be suspected to have diplopia attributable to perineural spread. Patients suffering from chronic alcoholism may develop Wernicke encephalopathy characterized by altered mental status, gait ataxia, and oculomotor dysfunction (ie, nystagmus and/or extraocular muscle weakness). A history of cardiovascular risk factors such as smoking, hypertension, hyperlipidemia, or diabetes is supportive of microvascular ischemia or vertebrobasilar insufficiency, although it is important not to assume cardiovascular risk factors exclude other serious neurologic disease.5
Giant cell arteritis may cause diplopia in patients over age 50. Associated systemic symptoms of giant cell arteritis (GCA) include jaw claudication, scalp tenderness, headaches, neck pain, ear pain, sudden hearing loss, myalgias, unexplained weight loss, fevers, or malaise. Rarely, patients with GCA may present with diplopia and without systemic symptoms.5,6
APPROACH/THE FOCUSED EXAM
History
The first step in evaluating a patient with binocular diplopia is to determine whether the patient has isolated diplopia or diplopia with additional neurologic deficits suggestive of a posterior circulation stroke. Patients presenting with acute onset diplopia in combination with altered mental status, bulbar weakness, vertigo, ataxia, or “crossed” brain stem signs (ipsilateral CN deficits with contralateral limb weakness or sensory loss) should be considered to have a brainstem stroke until proven otherwise.
The evaluation of patients with diplopia in the absence of acute onset brainstem symptoms begins with a focused history. The clinician should first determine the orientation of the diplopia (horizontal, vertical, or oblique) and whether the diplopia worsens in a particular direction of gaze. CN palsies and restrictive processes (such as thyroid eye disease or muscle entrapment by orbital fractures) cause incomitant diplopia, that is, diplopia that worsens in a particular direction of gaze corresponding with the affected extraocular muscle(s). By contrast, neuromuscular disorders such as myasthenia gravis may cause comitant (the same in all gaze directions) or incomitant diplopia.
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