Evaluation of the adult with diplopia

Evaluation of the adult with diplopia

Forrest D. Ellis

Zionsville, IN, USA

Introduction

An adult patient with new complaints of diplopia presents a diagnostic and therapeutic challenge to the treating physician. Virtually any condition known to produce diplopia can be responsible for the patient’s complaints, including longstanding but previously asymptomatic childhood disorders of ocular motility. Certain conditions such as multiple sclerosis, myasthenia gravis, myositis, and endocrine dysfunction are more common in adults than in children. An adult may acquire paresis or paralysis of one or more of the extraocular muscles through many mechanisms, including closed head trauma. Adults may acquire restrictions to movement of the extraocular muscles through direct muscle trauma, immune/ inflammatory disease, or endocrine disorders. A foundation for a patient’s recent acquisition of diplopia might have been laid by a pre-existing or congenital ocular motility problem. Separating these entities appropriately can be difficult.

As an example, an adult patient complaining of diplopia may have a complex history and physical examination. That patient may have a history of childhood strabismus and monocular occlusion, but no diplopia complaints until after a recent automobile accident during which closed head injury with brief unconsciousness occurred. Physical examination might reveal a minor decrease in visual acuity in one eye and small angles of horizontal and vertical strabismus with torsion. Prior records from earlier ocular examinations might not be available. Litigation regarding the automobile accident might be pending. The patient may not be working and may request relief from his diplopia via surgery so that he can settle the lawsuit and return to his work as a bookkeeper.

History

While a physician must be his patient’s advocate, he should not forget that he could inadvertently enter into a relationship with that patient which is based on assumptions rather than facts. The unwary physician can become the next person to be held responsible for a patient’s continued complaints, especially if he has performed one

Address for correspondence: Forrest D. Ellis, MD, 7182 Hunt Club Road, Zionsville, IN 46077, USA

At the Crossings: Pediatric Ophthalmology and Strabismus, pp. 157–168

Proceedings of the 52nd Annual Symposium of the New Orleans Academy of Ophthalmology, New Orleans, LA, USA, February 14-16, 2003

edited by Robert J. Balkan, George S. Ellis Jr. and H. Sprague Eustis © 2004 Kugler Publications, The Hague, The Netherlands

or more surgical procedures that have failed to relieve that patient’s diplopia, or have produced diplopia.

The history form, filled out by the patient in his handwriting, always is important. The patient should be queried directly by this form as to the nature of his complaints, the duration of those complaints, and the patient’s impression of the cause of those complaints. The physician should review this form, ask for details when necessary, and amplify the patient’s remarks via physician’s notes in the margins of the form. Any history of glasses wear in childhood may be important and should be noted. Monocular occlusion or the monocular application of eye drops as a child, any history of prior diplopia, or of strabismus surgery is notable. Any history of any other type of ocular or orbital surgery should be recorded including cataract, laser-assisted in-situ keratomileusis (LASIK), blepharoplasty, orbital decompression, and conjunctival surgery. Any history of surgery about the head and neck is important. Sinus surgery, especially endoscopic sinus surgery occasionally causes damage to extraocular muscles or to their innervation. Significant head trauma as a child should be noted. The patient should be queried specifically about prior treatment for hyperor hypothyroidism. Neurological history should be investigated in detail. Medications should be noted.

Family history

Strabismus in any family member can be relevant. Family photographs can be reviewed for glasses wear and head tilt. A driver’s license is almost always available for immediate review. Any family history of retinal degeneration or of mitochondrial disease is important.

Clinical examination

A thorough and appropriate ophthalmological examination should be carried out in all cases. Monocular diplopia must be excluded. The patient is asked to fixate a distance target and is then queried as to the presence or absence of diplopia. If diplopia exists, each eye is covered in turn and the question repeated. A patient with monocular diplopia will note that diplopia persists when one eye is covered, whereas a patient with binocular diplopia will note that diplopia disappears when either eye is covered.

A patient with monocular diplopia can then be tested with a pinhole. If monocular diplopia disappears when the patient views a distance target through a pinhole with that eye, it is presumed that optical aberrations or retinal receptor disturbance is responsible for the patient’s symptoms and the remainder of the examination is directed toward those areas. Special attention should be given to the cornea, lens, and foveal areas for clues to the explanation for monocular diplopia.

If the patient also has strabismus, prisms must be used to neutralize the angle(s) of the ocular deviations, and a judgment made as to the relative importance of monocular complaints versus binocular complaints.

When the patient’s diplopia is binocular, a thorough ocular examination is carried out. Often the usual ophthalmological examination must be extended to include gaze position measurements, assessment of ductions and versions, near point of accommodation in each eye, convergence amplitudes, stereoscopic testing, fusional amplitudes, visual fields, red lens, Maddox rod, Hess or Lee’s screen, Lancaster redgreen testing, color vision, exophthalmometer, and testing for aniseikonia.

Neurological dysfunction should be considered carefully. Often subtle neurological signs will accompany cranial nerve dysfunction and should be diligently sought in any case. If paresis or paralysis of one or more extraocular muscles is present, standard office techniques can elucidate the nature of the problem in most cases and further investigation can be specifically directed.

Specific disorders

Acquired paresis or paralysis of an extraocular muscle

An adult patient will complain of diplopia with maximum separation of images in the field of action of the paretic muscle. Red lens, Maddox rod, or Lancaster red-green testing will demonstrate this separation. Ductions will demonstrate underaction of the paretic muscle. Deviation of the visual axes will be greater when the patient fixates with the paretic eye (secondary deviation) than when he fixates with the normal eye (primary deviation.) Forced ductions will demonstrate no restrictions to passive movement of the globe and force generation tests will demonstrate reduced capacity of the muscle to generate the normal forces expected for eye movements. Saccadic velocities of the paretic muscle will be slowed. The patient may exhibit past pointing when fixating with the paretic eye if the paresis is of recent onset. An abnormal head position may be adopted. Associated neurological signs and symptoms should be sought.

If the paresis has existed over a longer period of time, all these relatively easy distinctions become less clear. The paretic muscle or its antagonist may become contracted or fibrotic and forced ductions may not remain entirely free. Gaze position measurements can become more uniform in all fields. An aberrant head position may be present. Separation of long-standing paresis from a restrictive disorder, such as that seen with milder degrees of thyroid ophthalmopathy, can be difficult.

Diagnostic evaluation may require computed tomography or magnetic resonance imaging of the head and orbits.

Convergence insufficiency or paralysis

Inability to converge adequately for near vision tasks is associated with diplopia at near in adults. Associated exotropia or intermittent exotropia may be present. Accommodative needs must be assessed and neutralized before concluding that a patient has convergence insufficiency. Convergence is thought to become more difficult in older patients, particularly in patients with an associated intermittent exodeviation. Diagnosis of convergence insufficiency can be difficult because convergence, in part, depends upon the effort exerted by the patient. Both functional and organic grounds for the apparent inability to converge exist. True or organic inability to converge (convergence paralysis) usually occurs suddenly and is characterized clinically by marked insufficiency or total lack of convergence, but with retention of medial rectus function on lateral gaze. Exotropia at distance is not present. The absence of convergence is usually associated with absence of miosis and lack of accommodation on viewing a near target (each component of the near reflex triad is affected).

Lesions of the dorsal brainstem in the region of the superior colliculi or of the occipital lobe are usually responsible for the patient’s inability to converge, and associated brain-

stem and occipital lobe signs can be present. Goldmann visual fields and imaging studies should be obtained when otherwise unexplained signs of inability to converge exist.

In general, treatment of convergence insufficiency is conservative and consists of near point exercises for younger patients and glasses and prisms for near tasks for older patients. In my experience, convergence exercises are of little use in older adults. Medial rectus resection can be performed, but results are variable and difficult to predict for the individual patient. Most adult patients with significant convergence insufficiency remain asthenopic, despite all forms of treatment. Single vision reading glasses with appropriate base-in prisms are helpful in some patients. Monocular viewing can be the best solution for near vision tasks in other patients.

Divergence insufficiency

A patient with sudden onset of divergence insufficiency will complain of diplopia at distance but not at near. Ductions may reveal mild underaction of each lateral rectus muscle. The distance deviation usually will measure 15 prism diopters of esotropia or less. A new onset of such symptoms should warrant a careful neurological examination, looking for other signs of neurological disease. Some cases progress to bilateral sixth nerve palsy. One study demonstrated that this condition resolved in a median of five months in as many as 40% of patients if associated neurological disease was not present.1 Treatment should be conservative until a stable deviation has been demonstrated. Both lateral rectus resection and medial rectus recession have been utilized with success.2

Skew deviations

Skew deviation refers to a hypertropia that cannot be explained on the basis of orbital disease or specific extraocular muscle innervation deficit. The vertical deviation may be concomitant or non-concomitant. A diagnosis of skew deviation is seldom made in the absence of associated brainstem or cerebellar signs. Thus, skew is felt to result from posterior fossa dysfunction, although no specific site for such a lesion has been demonstrated. It is usually seen with unilateral posterior fossa disease and the more hypotropic eye is thought to be ipsilateral to the site of the lesion.

When treated surgically, efforts are directed toward the mechanical realignment of the visual axes.

Convergence insufficiency, divergence insufficiency, and skew deviation have confounded ophthalmologists in many ways, and are often confused with other conditions producing diplopia. Inability to accurately localize the precise lesion causing these symptoms characterizes all three of these conditions.3

Adult onset of diplopia in patients with a long-standing history of strabismus

This is not an unusual presentation, but can be puzzling to the patient and physician. Sometimes seemingly incidental or trivial events can make an adult aware of diplopia, much as a child will suddenly discover physiological diplopia. However, an adult, once aware of diplopia, finds that avoiding diplopia can be difficult or impossible. Persistent diplopia is annoying and troublesome, although most adults eventually adjust to their ‘new’ angle of strabismus with eventual diminution in their symptoms.

Whether their adjustment is recovery of their ability to suppress the second image depends primarily on their ocular history and on the stability of their alignment. Most adults with new complaints of diplopia will choose to explore therapeutic options rather than allow diplopia to persist indefinitely.

The recent onset of diplopia in adult patients with a history of childhood strabismus usually is assumed to have resulted from some change in their angle of strabismus. A new problem such as cranial nerve palsy must always be ruled out. In the absence of a new problem, the optical axes are assumed to have moved from the usual position for that patient to the newer alignment with resultant diplopia. Diplopia may also result from a visual change in the patient’s job requirements. It is generally assumed that the ability to suppress or to ignore a diplopic image diminishes with age. Further, fusional amplitudes diminish with age, with a resultant reduction in the ability to control latent strabismus.

Change in alignment of the optical axes may occur for several reasons, including systemic illness, medication, trauma, refractive needs, cataract surgery, retinal surgery, and others. Office examination using prisms in free space, major amblyoscope measurements, tests for torsion, suppression and fusion can be reasonably predictive of whether or not the patient’s diplopia can be relieved via surgical intervention. Elimination of diplopia in such a patient may require precise alignment of the optical axes or the re-creation of a small angle of strabismus.

Recent adult extraocular muscle surgery with resultant diplopia

A thorough preoperative work-up with appropriate office testing will identify most adult patients with strabismus who are likely to experience troublesome diplopia if their existing strabismus is corrected surgically. This testing can be carried out during one or more office visits by using prisms in free space, or by asking the patient to wear Fresnel™ prisms on his glasses for a period of time preoperatively. Thirty-four percent (143/424) of adult strabismic patients so tested were found to have diplopia when their alignment was neutralized with prisms preoperatively.4 Only 40 (28%) of these at-risk patients developed diplopia postoperatively, however, and this diplopia persisted for less than six weeks. Three patients identified preoperatively as at risk for diplopia did develop intractable diplopia postoperatively. Based on these data, it would seem prudent to advise all adult patients with long-standing strabismus that realignment of their eyes could result in postoperative diplopia. For about 10% of these patients, this diplopia will be transient and will resolve in a few weeks. Intractable diplopia will develop in less than 1% of patients. Unfortunately, neither the patient nor the doctor can be sure preoperatively just who that 1% of patients might represent. It is especially important to remember that the postoperative alignment of the patient’s eyes must be precise and must include horizontal, vertical, and torsional alignment before it can be stated that the patient is incapable of fusion or suppression. Nevertheless, most patients with long-standing strabismus can be treated successfully. An overall success rate of 87% has been reported for treating such patients.5

Muscle slipped, ‘lost’, transected, or denervated

Occasionally, and for a variety of reasons, an extraocular muscle might slip within its capsule after apparently successful extraocular muscle surgery. In other cases, the muscle can become ‘lost’ or injured as a result of trauma, eye muscle surgery, or in

the course of a surgical procedure in the orbit or adjacent to the orbit. The injured muscle remains in the orbit, of course, but can be detached from the globe, pulled in two, transected, or denervated. An injured or detached muscle can be difficult to locate in the presence of significant tissue trauma, blood, and distorted anatomy. Computed tomography of the orbit often shows that the muscle spontaneously reattaches to sclera behind the equator of the globe. In these cases and in cases where the muscle retracts or slips within its capsule, the muscle can usually be located, secured, and reattached more anatomically by utilizing standard extraocular muscle techniques. In other cases, a muscle can be difficult or impossible to retrieve successfully via standard techniques. Successful muscle retrieval in these cases has resulted from using a variety of innovative measures, including transcutaneous medial orbitotomy approaches and transnasal endoscopic techniques.6-9 Muscle transfer procedures have to be considered when the muscle cannot be retrieved.

Cataract surgery

A variety of reasons exist that explain diplopia that is temporally related to cataract surgery. These reasons include pre-existing disorders, disorders produced by prolonged occlusion by the cataract, disorders produced by muscle injury in the course of the cataract surgery or anesthetic administration, and disorders resulting from the optical changes produced by the cataract removal and optical correction.10

It has been shown that local anesthetic agents and antibiotics injected into the orbit can infiltrate one or more of the extraocular muscles with resultant myotoxic or neurotoxic impairment of that muscle or muscles.11 The mechanism is presumed to include that of localized muscle edema and closed-compartment ischemia, followed by loss of elasticity and fibrosis of that muscle. Presumably, contracture of other extraocular muscles can occur depending on the patient’s fixation pattern and on specific muscle involvement. Pre-existing but asymptomatic conditions, such as thyroidassociated ophthalmopathy, have been shown to be responsible for many cases of diplopia following cataract surgery.12 Overaction of specific muscles, including the superior oblique muscle that are presumed to have been injected, has been reported, but this is not thought to be common and weakness of a muscle is the usual finding.13 Concomitant use of hyaluronidase with local anesthetic injections is thought to be somewhat protective in that hyaluronidase minimizes focal accumulation of the anesthetic agent.14

After the precise reason for post-cataract diplopia has been determined and optical aberrations treated appropriately, extraocular muscle surgery may be required. Successful treatment of non-optical diplopia after cataract surgery consists of watchful waiting for stability over a period of four to six months. During this interval, diplopia can be relieved utilizing press-on prisms or by occlusion. Surgical realignment can be successful, but many patients do require glasses, prisms, or ancillary treatment, even after extraocular muscle surgery.15

Refractive surgery

Diplopia can develop infrequently after LASIK or other forms of refractive surgery.16 This may occur because of vertical decentration of the corneal flap, ‘visual aberrations’, central islands, aniseikonia, unexpected refractive outcomes, or irregular astigmatism.17 Only a relatively small number of flaps (3.4% in one series)

are truly decentered.18 LASIK enhancement has been shown to be effective in correcting decentration.19 Rarely, diplopia occurs because of unrecognized preexisting strabismus that, after correction of the refractive error, becomes symptomatic.

Clinical trial of optical correction via a contact lens prior to surgery can be predictive of diplopia due to aniseikonia and, to some degree, of the patient’s ability to cope with this development. The New Awaya test for aniseikonia may be useful clinically for the determination of significant degrees of aniseikonia.20 Aniseikonia is treated with high index refraction lenses in most cases when it is symptomatic.21

Thyroid-associated ophthalmopathy

Milder forms of extraocular muscle involvement secondary to thyroid-associated eye disease are said to be the most easily overlooked causes of adult strabismus. All the extraocular muscles are involved in this disorder, but some muscles are more affected than others. In order of frequency, the inferior rectus, medial rectus, superior rectus, and lateral rectus muscles are involved. The oblique muscles are only rarely affected clinically to a significant degree. The usual history obtained from the patient is that of treatment for hyperthyroidism years previously, subsequent thyroid hormone replacement therapy, and gradual development of diplopia. Thyroid replacement therapy usually is evident from the patient’s medication list. Ductions will be limited, or lack of commitment will be apparent when gaze-position measurements are recorded. Proptosis may or may not be present. Ultrasound and computed tomography can be helpful in assessing the size and shape of the extraocular muscles, but are not always diagnostic. Surgical treatment is based on clinical findings, and may include orbital decompression followed by extraocular muscle surgery.

Retinal disorders

Compression or separation of retinal receptors in the foveal area from any cause can result in aniseikonia with diplopia.22 This may occur with macular degeneration, macular holes, and vitreoretinal traction. Vitreoretinal surgical intervention does not necessarily relieve the patient’s diplopia. Extraocular muscle surgery is seldom indicated because of the small angles of deviation. Prisms may be helpful in some cases, but are likely to produce only transient relief.

Retinal translocation surgery has produced dramatic improvement in visual acuity in many patients with various forms of macular degeneration. The improvement in visual acuity is often accompanied by large angle horizontal, vertical, and torsional diplopia, due to the non-anatomical position of the translocated retinal elements. Complaints of torsion and vertical diplopia characterize this condition.

So-called ‘full’ macular translocation, where the macula is moved 15-20 degrees, is more likely to induce large angle strabismus than ‘limited’ macular translocation, where scleral imbrication is performed with little movement of the fovea away from its usual anatomical location. Thirteen of 250 patients (5.2%) treated with limited translocation complained of postoperative diplopia.23 Diplopia resolved in ten of these 13 patients with prism therapy alone, but persisted in three patients who required occlusive lenses for diplopia relief. Prism and cover tests did not reliably quantify the deviations, and some diplopic patients had no discernible deviation of their eyes with cover testing.

Treatment options for ‘full’ macular translocation have included extraocular muscle surgery at the time of retinal surgery in an effort to prevent large angle deviations from occurring.24 Usually, however, surgical intervention for diplopia is delayed and the patient’s complaints are managed with prisms if possible. Prisms, of course, have little effect on the torsional aspect of the patient’s deviation. If surgical correction is undertaken, more than one surgical procedure can be required, and limited success can be expected. Due to the large cyclovertical components of the usual deviation, oblique muscle surgery often is performed. It is not likely that stereopsis will be recovered as a result of surgery in most of these cases.25 Surgery for ‘full’ macular translocation with resultant diplopia may be most useful for those patients who are essentially monocular, but who have special disorientation. However, isolated cases of recovery of stereopsis after extraocular muscle surgery in cases of limited macular translocations have been reported.26

More common reasons for diplopia associated with retinal detachment surgery are mechanical restrictions created by encircling bands and sponges that compromise or limit extraocular muscle movement.

Blepharoplasty, pterygium and extraocular muscle surgery

Blepharoplasty has resulted in diplopia secondary to extraocular muscle injury.27 It appears that the risk of diplopia may be increased when transconjunctival blepharoplasty is performed rather than transcutaneous blepharoplasty.

Pterygium surgery has resulted in injury to, or disinsertion of, the medial rectus muscle with resultant strabismus and diplopia.28

Inclusion cysts occasionally develop following extraocular muscle surgery and can be quite large.29 The precise etiology of these cysts is not always clear.30 Conjunctival elements are often identified in the cyst wall, and it is assumed that most of these are related to surgical technique.

Myasthenia gravis

While not limitedtoadults, myastheniagravistypicallypresentsin theadult population. Diplopia and ptosis are common presenting complaints, and myasthenic symptoms frequently are limited to the extraocular muscles and to the levator palpebrae superioris. A history of variability in symptoms is usually obtained. Thus, a patient might be symptom-free after a night’s sleep, only to develop increasing symptoms as the day progresses. A variety of diagnostic tests and therapeutic options are available to the examiner (see Childhood blepharoptosis, pp. 233-250). It should be noted that acetylcholine receptor antibody test results might be normal in as many as 71% of myasthenic patients whose symptoms are limited to the eyes.31

Myastheniapatientsoftenrequireextraocularmusclesurgeryorptosissurgery.Longstanding inactivity at the myoneural junction often leads to permanent dysfunction, with resultant paresis and contracture of the extraocular muscles and the levator muscle. Surgical success is quite good in such patients as long as their systemic status and medical management has been optimized.

Multiple sclerosis

Multiple sclerosis (MS) produces many ocular signs and symptoms, as well as generalized symptoms. The classic presentation of internuclear ophthalmoplegia is well known to ophthalmologists. MS may present with any combination of vertical, horizontal, and torsional diplopia. Diplopia may also occur in only one field of gaze. Isolated extraocular muscle palsy has been reported.32 Other central nervous system and midbrain signs of dysfunction are often present.33 Nystagmus may also be present. Stable strabismus originating from MS is occasionally treated with extraocular muscle surgery. I have treated six such patients surgically, with recovery of a useful diplopiafree field of vision in each patient. One patient eventually required a second surgical procedure after exacerbation of her MS.

MS has been reported in two patients who also had thyroid-associated ophthalmopathy and myasthenia gravis.34

Myositis

Inflammation may involve one or more of the extraocular muscles. The patient complains of pain on eye movement, and ductions are limited in the field of action of the involved muscle. Tenderness to palpation of the globe in the vicinity of the affected muscle is usually present. Some consider this condition to be a localized form of orbital pseudotumor.35 Response to systemic corticosteroids is considered to be confirmatory to the diagnosis if a dramatic reduction in symptoms occurs.

Other inflammatory disorders

Rheumatoid arthritis has been associated with the development of Brown’s syndrome in adults and with isolated extraocular muscle inflammation. Other types of orbital inflammation including vasculitis and necrotizing scleritis may affect the orbit and its contents.36-38

Tumors

Primary orbital tumors, particularly of the lacrimal gland, are not uncommon in adults. Further, the orbit is a metastatic site for several tumors.

My recent experience

The 100 most recent consecutive charts of adult patients for whom I had surgically attempted to realign their eyes were reviewed for age of the patient, diagnosis, and surgical result. Diagnoses listed are based on the surgeon’s clinical judgment as to the most likely explanation for the patient’s current condition. Diagnoses were arrived at via an assessment of the history, clinical examination, and imaging or laboratory studies when appropriate.

A variety of surgical procedures were employed. Unsatisfactory alignment postoperatively is defined as failure to achieve alignment in or around primary position to a degree that either the patient or the surgeon, or both, believe that further surgery or prism glasses are necessary. No patient required occlusion for relief of

postoperative diplopia. Several patients with satisfactory alignment around primary position continued to have diplopia in some field of gaze. No patient had ‘intractable’ diplopia in or around primary position. Some patients had residual amblyopia with suppression (Table 1).

Table 1. Clinical diagnoses in adults undergoing extraocular muscle surgery and results (n = 100; age range, 22-83 years; average age, 55.32 years)

Note: one patient had both thyroid-associated ophthalmopathy and myasthenia gravis

Summary

Adults develop diplopia for a wide variety of reasons. Symptoms must be correlated to clinical findings. Treatment options are numerous, but choices are largely dependent upon the underlying diagnosis and the general health of the patient. Extraocular muscle surgery can effectively relieve symptoms without creating a new problem in most of those patients for whom it is indicated.

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