Approach to Diplopia (Neuro-opthalmology October 2019)

Educational Objectives

The goal of this program is to improve diagnosis and management of neuro-ophthalmologic disorders. After hearing and assimilating this program, the clinician will be better able to:

1. Summarize and provide examples of the main categories of disorders included in the differential diagnosis of diplopia.
2. Use the neuro-ophthalmologic examination to distinguish among palsies of the cranial nerves that innervate the extraocular muscles.
3. Recognize historical factors that may lead to the diagnosis of myasthenia gravis in a patient presenting with diplopia.

Summary

Monocular diplopia: Most common causes of monocular diplopia are ocular surface dysfunctions such as dry eye, cataract, and undercorrected refractive error; clinician should ask patient to cover one eye; if diplopia persists, neurologic disorder unlikely (patient probably has refractive error); conversion disorder uncommon; most patients with nonorganic diplopia have binocular diplopia caused by convergence spasm.

Convergence spasm: Refers to overexpression of normal physiologic neurovisual process; when gaze shifted from distant object to close object (eg, computer, reading material), eyes must come together to remain focused (ie, converge); convergence associated with two other functions that allow focus on near target (constriction of pupils and change in thickness of lens); in some patients, eyes become “stuck” in convergence position; in such cases, eyes deviated in toward nose and patients describe blurred vision associated with overfocusing of lens.

Evaluation of binocular diplopia: Neurologic clinicians more likely to see patients with binocular than monocular diplopia; clinician should ascertain whether patient’s diplopia constant or intermittent; constant diplopia may be caused by structural lesion such as cranial nerve palsy; intermittent symptoms suggest failure of fusion caused by decompensated phoria or myasthenia gravis; clinician should ask about orientation of diplopia (side to side, vertical, oblique [or diagonal]), whether diplopia present at distance or up close, and whether degree of diplopia varies with direction of gaze; responses often allow clinician to determine cause of diplopia.

Decompensated phoria: Phoria refers to misalignment of eyes; mild strabismus common and may not be symptomatic until later in life; patients with history of minor head trauma (resulting from, eg, fall, sports injury, motor vehicle accident) often experience no immediate visual sequelae, but eyes may become misaligned in certain situations; patients may subconsciously compensate for phoria for some time but later experience diplopia; on examination, eyes may tend to become misaligned in vertical or horizontal direction such that patient experiences diplopia with fatigue or in setting of another illness (eg, uncomplicated upper respiratory infection, systemic disease).

Diplopia in distance versus near vision: Horizontal diplopia tends to be more pronounced at distance; diplopia that worsens at distance may be related to palsy of cranial nerve VI (eyes unable to diverge as patient switches from near to far vision); conversely, when diplopia more pronounced in near vision, patient has failure of convergence; palsy of cranial nerve III may limit adduction of eyes.

Examination of ductions: Patient may present with horizonal diplopia that worsens in left gaze; examiner should first assess ductions (eye movements) in each eye separately; clinician covers one eye and asks patient to follow target with other eye; examiner leads patient through cardinal positions of gaze, assessing ability to adduct and abduct fully.

Versions: Next, clinician should assess versions (eye movements with both eyes open); examiner again tests cardinal positions of gaze; testing eyes together allows clinician to detect asymmetry; for example, in patient with palsy of left cranial nerve VI, abduction of left eye less than that of right eye.

Alignment: Examiner then evaluates alignment using alternate cover test (patient fixes gaze on target across room; examiner moves paddle occluder or index card from one eye to other while looking for movement of uncovered eye as it focuses on target); as occluder moves, each eye should shift outward when gazing toward target in distance; in patient with palsy of left cranial nerve VI, degree of movement greatest when patient views object in left gaze; as patient turns head to right, eyes move to left, and weak left cranial nerve VI cannot fully abduct eye; as occluder sequentially shifts between eyes, greater shift back toward midline observed.

Pursuits and saccades: Pursuits indicate whether movements of eyes smooth and coordinated; with restrictive process in orbit such as thyroid orbitopathy, pursuits in one eye may be limited or “jerky”; testing of saccades (rapid eye movements from one direction of gaze to another) especially helpful for detection of internuclear ophthalmoplegia in patient with diplopia; patient with internuclear ophthalmoplegia exhibits slowed adduction in affected eye with saccades from eccentric gaze back to midline (often not detected by testing versions, ductions, and pursuits).

Causes of binocular diplopia: Divided into four categories (dysfunction of supranuclear and internuclear oculomotor control, dysfunction of nuclear and infranuclear oculomotor control, dysfunction at neuromuscular junction, and orbital disease).

Supranuclear diplopia: Typically associated with brain trauma, neoplasm, ischemia, or Parkinson disease (which may impair supranuclear control of gaze); such patients often have historical factors related to their diplopia (diplopia consequence of significant intracranial pathology).

Internuclear diplopia: Often associated with dysfunction of cranial nerve III, IV, or VI; knowledge of innervation and primary functions of extraocular muscles allows clinician to localize problem; horizontal diplopia related to cranial nerve III or VI; oblique (diagonal) diplopia (especially in downgaze) usually indicates problem with cranial nerve IV, which innervates superior oblique muscle.

Cranial nerve VI: Diplopia related to cranial nerve VI most often caused by microvascular lesion; condition typically seen in patients over 50 years of age with diabetes mellitus or dyslipidemia; small ischemic event may involve only cranial nerve VI; patient presents with binocular horizontal diplopia with symptoms more pronounced at distance and when direction of gaze toward affected side; palsy of cranial nerve VI may be associated with increased intracranial pressure (which may stretch cranial nerve VI, causing false palsy); funduscopic examination important in any patient with palsy of cranial nerve VI.

Cranial nerve III: Palsy may be traumatic or ischemic; aneurysm of posterior communicating artery may compress nerve, disrupting ocular motility; clinician should check for involvement of pupil and for ptosis (suggesting aneurysm).

Cranial nerve IV: Palsy most commonly congenital; patients often compensate with head tilt; old photographs or driver license may show head tilt, confirming congenital palsy; trauma another cause of palsy of cranial nerve IV; head trauma need not be of sufficient significance to cause loss of consciousness, fracture, or laceration.

Symptoms of nerve palsies: Microvascular infarction of cranial nerve III or VI sometimes associated with pain, discomfort, or change in sensation (eg, heightened awareness of eye or tissues surrounding eye); if pain major symptom, clinician should consider causes other than microvascular lesions.

Disorders of neuromuscular junction: Include myasthenia gravis (MG); two clues suggest MG may be etiology of diplopia (ie, intermittent or variable symptoms that worsen at certain times of day [eg, with fatigue late in day]; variable orientation of diplopia [sometimes horizontal and sometimes vertical]); family members should be asked about droopy eyelids; patient may report other transient or intermittent bulbar symptoms such as difficulty swallowing or weak voice when fatigued; MG has bimodal age distribution (half of patients present in their seventies or eighties); older patients presenting with diplopia sometimes misdiagnosed with stroke; MG can mimic any pupil-sparing cranial nerve palsy; patient with intermittent symptoms should be reexamined after 15 to 30 minutes of rest (change in pattern of diplopia strongly suggests MG).

Orbital disease: Thyroid orbitopathy — autoimmune condition associated with gradual increase in size of extraocular muscles caused by edema; muscles become boggy and less able to rotate globe in desired direction of gaze; patients gradually develop diplopia that does not localize to distribution of specific cranial nerve and may exhibit variable symptoms; edema often maximal on wakening and improves throughout day; enlargement of extraocular muscles over time may result in compression of optic nerve at orbital apex, leading to progressive loss of visual fields and optic neuropathy; visual field tests indicated in patient with known or suspected thyroid orbitopathy.

Management of diplopia: Clinician should treat underlying cause when possible; patient with thyroid orbitopathy or MG expected to improve when primary disorder treated; in other cases, patient may be advised to use eye patch or opaque tape over one side of spectacles (occluding one image may eliminate double vision); prism lenses — option for patients with stable diplopia (ie, exhibiting consistent pattern and degree); Fresnel (paste-on) prisms available in varying strengths; temporary prism used on one or both lenses of spectacles; once appropriate strength of prism determined, prism can be incorporated into eyeglasses; prism aligns eyes and eliminates symptoms; surgery — if misalignment significant or pattern inconsistent (diplopia varies with direction of gaze), patient may undergo repositioning of extraocular muscles; goal to eliminate double vision in primary position; patients with significant or incomitant misalignment may experience persistence of double vision when looking to side.

Summary: Systematic approach to diplopia focuses on neuroanatomy and localization; in most cases, diplopia not neurologic emergency; patient should be reassured that therapeutic strategies available.

Readings

Glisson CC. Approach to diplopia. Continuum (Minneap Minn) 2019;25(5 Neuro-ophthalmology).

Disclosures

For this program, the following was disclosed: Dr Glisson reports no disclosure.

Unlabeled Use of Products/Investigational Use Disclosure: Dr Glisson reports no disclosure.

To view disclosures of planning committee members with relevant financial relationships, visit: legacy.audio-digest.org/continuumaudio/committee. All other members of the planning committee report nothing to disclose.

The material presented in Continuum Audio has been made available by the AAN for educational purposes only and is not intended to represent the only method or procedure for the medical situations discussed but rather to present an approach, view, statement, or opinion of the speaker(s), which may be helpful to others who face similar situations. Opinions expressed by the speakers are not necessarily those of the AAN, its affiliates, or the publisher. The AAN, its affiliates, and the publisher disclaim any liability to any party for the accuracy, completeness, efficacy, or availability of the material contained in this program (including drug dosages) or for any damages arising out of the use or nonuse of any of the material contained in this program.

Acknowledgements

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

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Lecture ID:

CA080501

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.