Convergence Insufficiency

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Background

Convergence insufficiency is a common condition that is characterized by the inability to maintain proper binocular eye alignment on near objects.[1, 2] Patients with symptomatic convergence insufficiency report difficulty with near work, including blur at near, eye strain, or frank diplopia. Abnormalities on examination include exophoria or exotropia at near, reduced fusional vergence amplitudes, and an increased near point of convergence.[3] Convergence insufficiency is a common disorder in young and aging adults and may be isolated and idiopathic or associated with other neurologic disease.

Convergence is the disconjugate adduction of the eyes for vision of near targets. Appropriate convergence is necessary for clear binocular vision at near, and binocular foveation is essential for stereopsis. Convergence is a component of the near-response triad, along with accommodation of the lens and miosis. The primary stimulus for the near response is positional disparity of an image on the retina, with a smaller contribution from blurring of objects at near. These can be objectively measured by measuring the convergence response to accommodative stimuli (accommodative convergence to accommodation ratio [AC/A]) and the accommodative response to convergence stimuli (convergence accommodation to convergence ratio [CA/C]). Small imprecisions in this system can be compensated for by a cortical process called sensory fusion.[4] However, when convergence responses to near are sufficiently reduced, convergence insufficiency results.

Pathophysiology

Convergence insufficiency is a supranuclear disorder of ocular motility. In the cerebral cortex, the primary and secondary visual cortices respond to binocular disparity and depth. The secondary visual cortex can generate reflexive vergence eye movements. The right parietal lobe directs visual attention, and the frontal eye fields generate the signal for voluntary shifts from far to near targets, as well as tracking of approaching objects. Additional structures in the midbrain and pons are involved in these pathways and coordinating convergence eye movements with versions. Regions of the cerebellum contribute to near response and to smooth vergence tracking. The supraoculomotor area in the midbrain, adjacent to the oculomotor nuclei, is the final common pathway for convergence eye movements prior to the oculomotor nucleus.[4] Considering this distributed network, convergence insufficiency is typically poorly localizing and, as an isolated finding, is much more likely to result from an inherent imbalance within this system or decompensation secondary to multifocal cerebral dysfunction. This imbalance may be provoked by a reduction in the accommodative stimulus for vergence, as in presbyopic patients with new correction for near acuity.

Considering the interactions between the vergence and accommodative responses to similar stimuli, it is not surprising that both vergence and accommodation may be affected.[5]

Epidemiology

Frequency

United States

In children, the prevalence of convergence insufficiency is estimated at 4.2%-6%. In adults, the annual incidence is 8.4 per 100,000 population. By the ninth decade of life, approximately 70% of individuals may be affected.[6] The incidence increases with additional near work demand.

Convergence insufficiency is reported to be rare in children younger than 10 years. However, the increased visual demands of schoolwork and prolonged periods of reading exacerbate symptoms in older children.[7]

International

The prevalence of convergence insufficiency is the same in all industrial societies.

Mortality/Morbidity

The morbidity of convergence insufficiency relates to the near point visual demands of the patient's activities. Eye strain, fatigue, frequent loss of place while reading, and frank binocular diplopia associated with near point tasks are among the reported symptoms of convergence insufficiency.

Race

Convergence insufficiency has no racial predilection.

Sex

Convergence insufficiency has no sexual predilection.

Age

The frequency of convergence insufficiency symptoms may increase with age as patients' ability to compensate for their relative divergent binocular alignment decreases with time.

Prognosis

The prognosis of convergence insufficiency is excellent in most patients, as conservative therapies can be quite effective. However, approximately one quarter of patients have significant increases in the near exodeviation 20 years from diagnosis. A small percentage of patients may require surgery or resort to monocular occlusion at near.[6]

Patient Education

Patients should be made aware that convergence insufficiency is a fairly common condition and that treatment is generally effective.

History

Individual patients with convergence insufficiency may report a wide range of symptoms, including blur, motion of the visual target, eye strain, headache during near work, or diplopia. Difficulty reading or attending to near work is reported, either in isolation or accompanied by further descriptors. A standardized questionnaire, the Convergence Insufficiency Symptom Survey, was established for research purposes but may be helpful in identifying symptoms, although it lacks specificity as a screening tool.[8, 9, 10] Particularly in children, it may also be helpful to confirm symptoms with a range of activities rather than just required reading.[11]

Patients with convergence insufficiency often present as teenagers or in early adulthood, reporting gradually worsening eyestrain, blurred vision after brief periods of reading, and, sometimes, diplopia with near work. It is not unusual for the patient to squint or close one eye while reading to relieve blurring or diplopia. Few, if any, symptoms are present at distance fixation. Symptoms are aggravated by illness, sedative-hypnotic medications, lack of sleep, anxiety, and prolonged near work.[12]

The symptoms of convergence insufficiency are directly associated with reading or other near work visual demands. Many patients with objectively measured convergence insufficiency may not report symptoms. The clinician should inquire about any avoidance behavior in patients who are asymptomatic despite clinical findings consistent with convergence insufficiency.[13, 14] The most common symptoms associated with convergence insufficiency include asthenopia (eyestrain) and headache during near work, diplopia, blurred vision, and perceived moving of print while reading.[15]

Asthenopia (eyestrain)

These symptoms were clearly described by von Graefe as early as 1855. Typically, such symptoms occur after short periods of reading or other close work. This most frequently occurs because of the sustained increased effort required to increase fusional convergence.

Diplopia

The diplopia that manifests in patients with convergence insufficiency may present as two separate or overlapping images (a "ghost" image). Some patients describe blurry rather than double vision, but they may be able to identify that symptoms resolve with closure of either eye. These nondiplopic binocular symptoms are easily diagnosed in the symptomatic patient by checking monocular eye closure, which alleviates binocular symptoms.

Some patients with convergence insufficiency do not have symptoms of diplopia despite an obvious exodeviation at near. This may result from suppression of the nonfixating eye.

Blurred vision

Efforts to increase convergence through stimulation of accommodative convergence to eliminate diplopia can sometimes cause blur by simultaneously producing refractive error via over-accommodation.

Moving of print while reading

A sense of letters moving while reading may result from unstable binocular alignment relative to the near vision convergence demand. This usually occurs when the patient is unable to maintain sufficient fusional convergence to establish and maintain binocular vision, with visual attention alternating between competing eyes.

Physical

The cardinal signs of convergence insufficiency include an increased near point of convergence, decreased fusional convergence amplitude, and exodeviation greater at near.

Near point of convergence is tested by bringing a fixation target toward the patient and observing for the loss of binocular fixation. When the patient reports diplopia or loses binocular fixation, this is the near point of convergence. Norms for the near point of convergence increase during childhood, and various distances have been suggested as cutoffs for normal values. However, the 6-cm measure used by the Convergence Insufficiency Treatment Trial seems reasonable given limited normative data.[3, 16, 17] The authors of this article find the near point of convergence to be the least objective of the testing methodologies used for vergence dysfunction, as it is extremely effort dependent.

Positive fusional convergence amplitude is measured by placing increasing power of base-out prism in front of either of the patient’s eyes while they focus on a distant target. The maximum prism at which either the patient is observed to lose binocular fixation or reports diplopia is the positive fusional vergence amplitude. Healthy patients have prism diopter convergence amplitude of more than 15. Sheard’s criteria state that healthy individuals should have a convergence amplitude twice the magnitude of near phoria measured at 40 cm.[4, 3]

Ocular alignment tested via alternate cover reveals an exophoria at near that is ≥4 prism diopters greater than at distance.

Patients may demonstrate reduced stereoacuity at near.

Monocular near visual acuity should also be evaluated.

Causes

Convergence insufficiency is often seen in healthy children or aging patients. It has been proposed that the introduction of plus lenses for presbyopia may reduce accommodative stimuli for convergence; however, this was not shown in a population-based cohort.[6] Mild traumatic brain injury may be associated with subsequent convergence insufficiency.[18] More than 40% of patients with sports-related concussion demonstrated an abnormal near point of convergence.[19] Neurodegenerative diseases, including Parkinson disease and progressive supranuclear palsy, also cause convergence insufficiency. In Parkinson disease, decreased convergence amplitudes have been demonstrated early in the disease course.[20] Improvement of convergence with levodopa treatment has been reported.[21] Centrally acting medications also contribute to vergence dysfunction.[4]

While isolated impairment of convergence due to discrete brainstem lesions is rare, it has been reported. It can also occur with lesions of the medial longitudinal fasciculus causing internuclear ophthalmoplegia or with the dorsal midbrain syndrome, although convergence excess is more common in this scenario, and additional features are uniformly present on exam, assisting in the diagnosis.[4]

Patients with uncorrected hyperopia in excess of +5.00 diopters (D) may generate little or no accommodative effort at near.

Patients with mild-to-moderate myopia do not need to stimulate accommodation to see clearly at the usual near working distance in their uncorrected state. This lack of accommodative effort may result in decreased accommodative convergence.

Laboratory Studies

Usually, no laboratory studies are indicated. However, if there is suspicion for another disorder, such as those listed in the differential diagnoses based on clinical findings, appropriate laboratory testing should be conducted.

Imaging Studies

As with laboratory studies, imaging is not necessary unless there is concern regarding another disease process.

Medical Care

Convergence exercises (ie, orthoptics, vision therapy) and/or base-in prisms are the mainstays of treatment for convergence insufficiency.[25]

Orthoptics and vision therapy

The most commonly prescribed treatment is home-based exercises, such as pencil push-ups, although specific methodologies vary among practitioners.[6, 26] Pencil push-ups require fixation on a near target such as the number on a pencil and repeatedly bringing it from an arm’s length away toward the nose while maintaining fusion and focus until blur/diplopia is noted.

Home-based computer therapy involves specialized software to stimulate either convergence or convergence and accommodative responses. The putative benefits would include the opportunity for daily therapy while allowing for more structure than pencil push-ups, as well as the ability to monitor compliance. These have been shown to be beneficial in ameliorating both the signs and symptoms of convergence insufficiency.[27]

Office-based therapy provides a more structured environment and does not preclude the use of additional home-based exercises. It allows for the use of additional specialized equipment, such as base-out prism reading and stereogram cards, under the supervision of an orthoptist or a vision therapist. Different techniques can selectively induce and train responses to accommodative or vergence stimuli. It has been demonstrated that these exercises can result in changes in the coupling between accommodation and vergence responses.[28] No uniformly agreed upon standardized protocol for office-based therapy exists.[29]

Base-in prisms for near correct for ocular misalignment and can reduce accommodative overaction. These prisms can be ground into a separate pair of reading glasses, or Fresnel prisms can be fitted over the reading segment of the patient's bifocals.

A 2011 Cochrane review concluded that office-based therapy was more effective than home-based exercise or computer-based therapy in children. In adults, office-based therapy was more effective in treating clinical signs but not symptoms. In children, neither home-based approach was effective for symptoms, while computer therapy was superior with regards to clinical signs. This same review also assessed limited trials for base-in prisms and concluded that there may be a benefit in adults, although results were not superior to placebo in children.[30]

Refractive correction to monovision may also be helpful in treating the symptoms of convergence insufficiency.

Surgical Care

Numerous surgical techniques are available to patients in whom conservative treatment fails, including various forms of bilateral lateral rectus recession, bilateral medial rectus resection, and lateral rectus recession with medial rectus resection. However, given the efficacy of conservative treatment and the invasive nature of surgical intervention, conservative measures should be fully explored.[31] It should also be noted that, postoperatively, prisms may yet be required for overcorrection esotropia or residual or recurrent exodeviation.[32, 33, 34]

Activity

Patient activities are not restricted.

Prevention

Since the underlying etiology of convergence insufficiency is unclear, no specific recommendations can be given to prevent it. Avoidance of near work is often both undesirable and impractical.

Long-Term Monitoring

A combination of in-office and at-home orthoptics and vision therapy probably represents the best therapeutic approach for convergence insufficiency.[30, 35] Follow-up depends on the severity of symptoms and the treatment modality or modalities pursued.

Medication Summary

No medications are indicated for convergence insufficiency.

Author

Eric R Eggenberger, DO, MS, FAAN, Professor, Vice-Chairman, Department of Neurology and Ophthalmology, Colleges of Osteopathic Medicine and Human Medicine, Michigan State University; Director of Michigan State University Ocular Motility Laboratory; Director of National Multiple Sclerosis Society Clinic, Michigan State University College of Human Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: LifeBlood<br/>Serve(d) as a speaker or a member of a speakers bureau for: Biogen; Genzyme; Novartis; Teva; Mallinckrodt<br/>Received research grant from: Biogen; Genzyme; Novartis<br/>Received consulting fee from Biogen for consulting; Received consulting fee from Teva for consulting; Received consulting fee from Acorda for consulting; Received grant/research funds from Novartis for independent contractor; Received honoraria from Genentech for speaking and teaching; Received honoraria from Genzyme for speaking and teaching.

Coauthor(s)

Anthony J Brune, III, DO, Clinical and Research Fellow, Vestibular and Ocular Motor Otoneurology, Division of Neuro-Visual and Vestibular Disorders, Johns Hopkins University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

J James Rowsey, MD, Former Director of Corneal Services, St Luke's Cataract and Laser Institute

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Michael J Bartiss, OD, MD, Medical Director, Ophthalmology, Family Eye Care of the Carolinas and Surgery Center of Pinehurst

Disclosure: Nothing to disclose.

Richard W Allinson, MD, Associate Professor, Department of Ophthalmology, Texas A&M University Health Science Center; Senior Staff Ophthalmologist, Scott and White Clinic

Disclosure: Nothing to disclose.

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