iodide) decrease accommodative convergence. These drugs act directly on the ciliary body, facilitating transmission at the myoneural junction. They reduce the central demand for accommodative innervation and thus reduce the amount of convergence induced by accommodation. In the past, echothiophate was sometimes used to treat patients with high AC/A esotropia. This agent, which is associated with some systemic and ophthalmic complications (eg, development of iris cysts, cataracts; increased response to depolarizing muscle relaxants), is no longer commercially sold in the United States and is now used only rarely.
Surgery. Surgical management of high AC/A esotropia is controversial. Some ophthalmologists advocate surgery (medial rectus muscle recessions with or without posterior fixation or pulley fixation) to normalize the AC/A ratio, which may allow for discontinuation of bifocals and use of contact lenses. The risk of overcorrection at distance is small (<10%). Prism adaptation for the near deviation, the preoperative use of prisms to determine the maximum deviation, is used by some ophthalmologists.
Observation. Many patients show a decrease in the near deviation with time and ultimately develop binocular vision at both distance and near fixation. Some ophthalmologists observe the near deviation as long as the distance alignment allows for the development of peripheral fusion.
For the long-term management of both refractive and high AC/A accommodative esotropia, it is important to remember that measured hyperopia usually increases until age 5–7 years before it starts to decrease. Therefore, if the esotropia with glasses increases, the cycloplegic refraction should be repeated and the full correction prescribed.
If glasses or medication corrects all or nearly all of the esotropia and if some degree of sensory binocular cooperation or fusion is present, the clinician may begin to reduce the strength of the glasses to create a small esophoria, which is thought to stimulate fusional divergence. An increase in the fusional divergence combined with the natural decrease of both the hyperopia and the high AC/A ratio may enable the patient to eventually maintain straight eyes without bifocals or glasses altogether.
Partially accommodative esotropia
Treatment of partially accommodative esotropia consists of strabismus surgery for the deviation that persists while the patient wears the full hyperopic correction. It is important that the patient and parents understand before surgery that its purpose is to produce straight eyes with glasses—not to allow the child to discontinue wearing glasses altogether. In older patients, refractive surgery can be considered to both reduce the hyperopic refractive error and improve the ocular alignment. Results of these procedures for partially accommodative esotropia are not as impressive as those for pure refractive accommodative esotropia.
Acquired Nonaccommodative Esotropias
Basic Acquired Nonaccommodative Esotropia
Comitant esotropia that develops after age 6 months and that is not associated with an accommodative component is called basic acquired nonaccommodative esotropia. As in infantile esotropia, the amount of hyperopia is not significant, and the deviation is similar at distance and near. Acquired esotropia may be acute in onset. In such cases, the patient immediately becomes aware of the deviation and may have diplopia. A careful motility evaluation is important to rule out an accommodative or paretic component. Temporary but prolonged disruption of binocular vision—such as may result from a hyphema, preseptal cellulitis and mechanical ptosis, or prolonged patching for amblyopia—is a known precipitating cause of acquired nonaccommodative esotropia. In patients with acquired
nonaccommodative esotropia, fusion is thought to be tenuous, so this temporary disruption of binocular vision upsets the balance, resulting in esotropia.
Because the onset of nonaccommodative esotropia in an older child may be a sign of an underlying neurologic disorder, neuroimaging and neurologic evaluation may be indicated when other symptoms or signs of neurologic abnormality are present, such as lateral incomitance, deviation greater at distance than near, abnormal head position, diplopia, or concomitant headache. Many patients with acquired nonaccommodative esotropia have a history of normal binocular vision; thus, the prognosis for restoration of single binocular vision with prisms and/or surgery is good. Therapy consists of amblyopia treatment, if needed, and surgical correction or botulinum toxin injection as soon as possible after the onset of the deviation. The Prism Adaptation Study showed a smaller undercorrection rate (approximately 10% less) with surgery based on the prism-adapted angle.
Jacobs SM, Green-Simms A, Diehl NN, Mohney BG. Long-term follow-up of acquired nonaccommodative esotropia in a population-based cohort. Ophthalmology. 2011;118(6):1170–1174. Epub 2011 Jan 26.
Repka MX, Connett JE, Scott WE. The one-year surgical outcome after prism adaptation for the management of acquired esotropia. Ophthalmology. 1996;103(6):922–928.
Cyclic Esotropia
Cyclic esotropia is rare, with an estimated incidence of 1:3000–1:5000 strabismus cases. Onset typically occurs during the preschool years. The esotropia is comitant and occurs intermittently, usually every other day (48-hour cycle). Variable intervals and 24-hour cycles have also been documented.
Fusion and binocular vision are usually absent or defective on the strabismic day, with marked improvement or normalization on the orthotropic day. Diplopia on strabismic days can occur and is more often a prominent symptom in patients whose onset of esotropia occurred at a relatively older age and who are unable to develop suppression. Occlusion therapy may convert the cyclic deviation into a constant one.
Surgical treatment of cyclic esotropia is usually effective. The amount of surgery is based on the maximum angle of deviation present when the eyes are esotropic.
Sensory Esotropia
Monocular vision loss from various causes (eg, cataract, corneal clouding, optic nerve or retinal disorders) may cause sensory (deprivation) esotropia.
Obstacles preventing clear and focused retinal images and symmetric visual stimulation must be identified and remedied promptly, if possible. When marked abnormalities such as total unilateral congenital cataract are present, animal and clinical data indicate that restoration of the best-possible visual input must be accomplished at an early age if irreversible amblyopia is to be avoided. If surgery or botulinum toxin injection is indicated for strabismus, it is generally performed only on the eye with a significant deficit.
Divergence Insufficiency
The characteristic finding of divergence insufficiency is an esodeviation that is greater at distance than at near. The deviation is comitant in vertical and horizontal gaze, and fusional divergence is reduced. Divergence paralysis may represent a more severe form of divergence insufficiency. Because true paralysis of divergence cannot generally be documented, the term divergence insufficiency is preferred. Divergence insufficiency can be divided into a primary, isolated form and a secondary form associated with neurologic abnormalities, including pontine tumors, increased
intracranial pressure, or severe head trauma. In these secondary cases, the divergence insufficiency is probably due to sixth nerve paresis that is so mild that the abduction deficit has not yet become clinically evident. A thorough clinical evaluation can frequently distinguish between the 2 forms of divergence insufficiency. Primary, isolated divergence insufficiency is a benign condition that predominantly occurs in patients older than 50 years; symptoms sometimes resolve within several months. Patients with secondary divergence insufficiency require neuroimaging to rule out treatable intracranial lesions. Treatment of the underlying neurologic disorder (eg, corticosteroids for temporal arteritis, treatment of intracranial hypertension) may relieve symptoms. Management of diplopia consists of base-out prisms, botulinum toxin injection of the medial rectus muscles, and strabismus surgery.
Spasm of the Near Reflex
Spasm of the near reflex (also known as ciliary spasm or convergence spasm) is a spectrum of abnormalities of the near response. Patients present with varying combinations of excessive convergence, accommodation, and miosis. The etiology is generally thought to be functional, related to psychological factors such as stress and anxiety. In rare cases, it can be associated with organic disease. Patients may present with acute esotropia alternating at other times with orthotropia. Substitution of a convergence movement for a gaze movement on horizontal versions is characteristic. Monocular abduction is normal in spite of marked abduction limitation on version testing. Pseudomyopia may occur.
Treatment consists of cycloplegic agents such as atropine or homatropine, hyperopic correction for patients with significant hyperopia, and bifocals. Counseling to address underlying issues that are triggering this response may be helpful. Botulinum toxin injections of the medial rectus muscles and strabismus surgery can be considered with caution if the spasm cannot be broken.
Kaczmarek BB, Dawson E, Lee JP. Convergence spasm treated with botulinum toxin. Strabismus. 2009;17(1):49–51.
Consecutive Esotropia
Esotropia following a history of exotropia is called consecutive esotropia. It can be a spontaneous event or it can develop after surgery for exotropia. Spontaneous consecutive esotropia is rare and almost always occurs in the face of neurologic disorders, such as cerebral palsy, or with very poor vision in 1 eye. Postsurgical consecutive esotropia, on the other hand, is not uncommon. Fortunately, it often resolves over time. In fact, an initial small overcorrection is desirable after surgery for exotropia, as it is associated with an improved long-term success rate. Treatment options for consecutive esotropia, whether spontaneous or persistent postoperatively, include base-out prisms, hyperopic correction, alternating occlusion, botulinum injection, and strabismus surgery. In postsurgical consecutive esotropia, unless the deviation is very large or a slipped or lost muscle is suspected, surgery or botulinum toxin injection should be postponed for several months because of the possibility of spontaneous improvement.
A slipped or lost lateral rectus muscle produces varying amounts of esotropia, depending on the amount of slippage, and should be suspected in consecutive esotropia following lateral rectus recession surgery if a significant abduction deficit is present. However, if the ipsilateral medial rectus muscle was resected at the time of the lateral rectus recession, the consecutive esotropia could be due to a tight medial rectus muscle. Forced-duction testing helps differentiate between these two causes. In cases of a slipped or lost lateral rectus muscle, surgical exploration is required. Transposition procedures may be necessary when lost muscles cannot be found. For slipped muscles, the true muscle should be identified and secured with a suture, the pseudotendon attached to the sclera