A Review of Ocular Myasthenia Gravis and Its Differential Diagnoses

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doi: 10.62055/62817355Gm

ABSTRACT

BACKGROUND

Myasthenia gravis is an uncommon neuromuscular disease that often will present first to eye care providers, given that about half of patients have ocular symptoms as their first symptom of the disease. Myasthenia gravis is notorious for being a challenging diagnosis to make as the condition can have a variety of presenting symptoms that often mimic other more common conditions. Eye care providers serve an important role in identifying these patients and getting them referred to the appropriate specialists for management of their symptoms.

CASE REPORT

A 57-year-old Caucasian male presented to the VA eye clinic with a complaint of a new-onset ptosis that worsened over the course of the day. Upon exam, it was noted that he had pupillary miosis on the same side. Horner’s Syndrome was suspected and apraclonidine 0.5% was instilled without a change in pupil size. Forced eyelid closure test was then performed due to suspicion of myasthenia gravis with a positive result. He was then tested serologically and was positive for anti-AChR antibodies and successfully treated with pyridostigmine by neurology.

CONCLUSION

Myasthenia gravis can be difficult to diagnose but, with proper suspicion and testing, a diagnosis can be made in the examination room. Ocular myasthenia gravis is often the presenting manifestation of the disease and will often convert to generalized myasthenia gravis within the first few years of diagnosis. Eye care providers should make appropriate referrals for these patients to improve their symptoms and quality of life, especially given the several treatment options available that are generally well-tolerated and effective.

Keywords: myasthenia gravis, ptosis, diplopia

INTRODUCTION

Myasthenia gravis is a neuromuscular disorder that can be challenging to diagnose and can often first present with ocular findings including ptosis or diplopia. Understanding the different diagnostic tests and their sensitivity and specificity is imperative in managing patients with this condition, which can vary in ocular and systemic symptoms. This case reports on the presentation, diagnosis and treatment of an individual with ocular myasthenia gravis.

CASE REPORT

A 57-year-old Caucasian male presented to the eye clinic as a new patient with the chief complaint of a swollen right eye for two weeks. Upon further discussion, it was determined that he was reporting a drooping eyelid, rather than true periorbital or eyelid edema, that worsened at the end of the day. He denied symptoms of dysphagia, dyspnea, fever, headache, diplopia, or facial anhidrosis. He denied a history of recent head or neck surgery or manipulations. His medical history was significant for type II diabetes mellitus, esophageal stricture, hypertension, and hyperlipidemia. His current medications included amlodipine besylate, empagliflozin, metformin, chlorthalidone, hydroxyzine, benazepril, rosuvastatin, and glimepiride. He denied any ocular history or trauma and had been using over-the-counter readers.

His visual acuities were 20/20 in each eye with refraction. Upon examination, asymmetry in palpebral aperture height was noted (right eye 5 mm, left eye 9 mm) in addition to anisocoria with the smaller pupil on the right side. In bright light, his pupil sizes were right eye 3 mm and left eye 4 mm. In the dark, his pupil sizes were 4 mm and 5 mm for the right and left eyes, respectively, without a lag in dilation. Pupils reacted to light appropriately and no afferent pupillary defect was noted. He had full range of motion upon motility testing and visual fields were full to finger count.

The forced eyelid closure test was performed next. After a short period of forced eyelid closure, the right upper eyelid had an initial resolution of ptosis with similar palpebral aperture height to the left eye (9 mm) that gradually fell to its original palpebral aperture height of 5 mm.

Given that the patient presented with new-onset ptosis with ipsilateral miosis, pharmacological evaluation for Horner’s Syndrome was performed. This decision was made given the important prognostic implications that a diagnosis of Horner’s Syndrome holds, in addition to the ease of testing in office. There was no change in palpebral aperture height or pupil size after apraclonidine instillation, which also lessened the suspicion of Horner’s syndrome. Finally, the anisocoria was equal in dim and bright environments, further providing evidence to point to physiological anisocoria.

Further examination included intraocular pressure of 20 mmHg and 18 mmHg in the right and left eyes. Dilated fundus examination was performed with tropicamide 1%. His optic nerves each had C/D of 0.50 round with healthy rims and his fundus examination was unremarkable for maculopathy, vasculopathy, or peripheral retinal findings.

Ocular myasthenia gravis was suspected in this patient that presented with recent-onset ptosis of the right eye that worsened with fatigue and had a positive forced eyelid closure test. Serologic testing for myasthenia gravis was ordered and included acetylcholine receptor binding antibody, striated muscle antibody screen, acetylcholine receptor modulating antibody (anti-AChR), and anti-muscle-specific kinase antibodies (anti-MuSK). Given the systemic implications of Horner’s syndrome and the easy access to radiologic testing, a chest x-ray was also ordered to evaluate for Pancoast tumor, which was negative. Results for serologic testing came back within several weeks and are summarized in Table 1.

Table 1: Serologic testing results.

The serologic testing combined with in-office clinical tests were consistent with myasthenia gravis. A consult to neurology was placed and a chest CT ordered to evaluate for the presence of a thymoma. Between his appointment with optometry and neurology, he called in to report the new development of intermittent diplopia with stable right ptosis. He was seen by neurology a month later and they reported his findings were more consistent with ocular myasthenia and less likely generalized myasthenia gravis as he did not have any systemic symptoms. Pyridostigmine treatment was initiated at a dose of 60 mg three times daily. At his one-month follow-up appointment, he noted complete resolution of his ptosis and near-complete resolution of his diplopia, though this would still occur on occasion with fatigue. He was then lost to follow up.

DISCUSSION

Myasthenia gravis is an uncommon neuromuscular condition characterized by autoantibody production against post-synaptic receptors or proteins within the neuromuscular junction. An annual incidence of 9-10 cases per million persons and an annual prevalence of 150-250 cases per million persons has been reported.¹ Both prevalence and incidence rates are rising, likely due to improvements in diagnosis and patient longevity. The hallmarks of myasthenia gravis include muscle fatigability and variability of symptoms. The clinical course of the disease can be diverse and is often dependent on the specific autoantibody produced. Many cases (50-85%) will present with ocular symptoms, meaning that it is often eye care providers who have the first opportunity to suspect and test for the disease.^1-3

Ocular myasthenia gravis (OMG) is characterized by a patient presenting solely with ocular symptoms, such as fluctuating ptosis, diplopia, and orbicularis weakness. Generalized myasthenia gravis (GMG) is defined by any symptoms beyond the extraocular muscles or eyelids, including dysphagia, dysarthria, dyspnea, dysphonia, and neck or extremity weakness.⁴ The reported transformation rate of OMG to GMG varies between 20-85% across different studies.³ However, there seems to be a consensus that slightly more patients will convert to GMG than remain as OMG. Factors that increase the likelihood of conversion include seropositivity for anti-AChR (67%), presence of thymoma (10-15% of cases), and positive single-fiber electromyography at diagnosis (77%).^3,5 In a population-based study, 55% of patients converted from OMG to GMG at some point in the course of the disease. Of the patients that did convert, most did so within the first two years (50% at one year, 72% at two years, and 94% within five years).³

Serologic testing is often subsequently ordered to confirm a diagnosis of myasthenia gravis and determine the responsible autoantibodies, which can give the doctor and patient insight into the clinical course of the disease. Additionally, most patients (92%) with confirmed myasthenia gravis will develop ocular symptoms at some point within the course of their disease.²

PATHOPHYSIOLOGY

Upon excitement of a skeletal muscle nerve fiber, acetylcholine is released from the presynaptic membrane via voltage-dependent calcium channels into the synaptic cleft. Acetylcholine then diffuses through the synaptic cleft to the postsynaptic membrane where acetylcholine receptors (AChR) are present in clusters. The binding of acetylcholine to these receptors results in depolarization and subsequent muscle contraction. Once completed, acetylcholinesterase will facilitate the cleaving of acetylcholine into acetic acid and choline to later be reused within the presynaptic terminal.

In myasthenia gravis, autoantibodies interfere with the functioning of the postsynaptic membrane within the neuromuscular junction. Acetylcholine receptors are supported by two key proteins: muscle-specific kinase (MuSK), which stimulates the clustering of acetylcholine receptors, and lipoprotein receptor-related protein 4 (LRP4), which cleaves acetylcholine into acetic acid and choline to be reused within the presynaptic terminal. Without proper function of all three of these postsynaptic components, skeletal muscle weakness and fatigability occur. Currently, there are three autoantibodies known to be involved in myasthenia gravis: acetylcholine receptor antibodies (anti-AChR), muscle-specific kinase antibodies (anti-MuSK), and lipoprotein receptor-related protein 4 antibodies (anti-LRP4).

DIFFERENTIAL DIAGNOSES

Myasthenia gravis can be a notoriously elusive diagnosis, especially in cases that present with either ptosis or diplopia given the broad range of possible causes. However, it is important to remember that the hallmark of myasthenia gravis is a fluctuating degree of muscle weakness that is often worse at the end of the day or after prolonged usage.

Ptosis Only

Variable ptosis in the absence of diplopia is a common finding in myasthenia gravis (21%).² Horner’s Syndrome should be considered in cases presenting with a mild ptosis. Horner’s Syndrome is known for a particular triad of signs: ipsilateral ptosis, miosis, and anhidrosis. This patient presented with both a mild ptosis and miosis of the same side. He denied anhidrosis, though the degree of anhidrosis in Horner’s Syndrome can vary quite widely and is often difficult for patients to detect. Despite pupil testing being consistent with physiological anisocoria the decision was made to instill apraclonidine at his initial visit given the prognostic implications – such as Pancoast tumor and carotid artery dissection – as well as the simplicity of the test. Apraclonidine in Horner’s Syndrome will result in “reverse anisocoria,” where the affected pupil will dilate due to denervation hypersensitivity to apraclonidine, whereas a normal pupil will not dilate. In some cases, this may also be accompanied by a reversal of the ptosis. The size of the patient’s pupils and degree of ptosis was unchanged after apraclonidine instillation, which further reduced the suspicion for Horner’s Syndrome.  A complete ptosis should raise suspicion for a third cranial nerve palsy, which is discussed in greater detail below.

Diplopia Only

Cases presenting with diplopia alone (27%) can be the most challenging to suspect myasthenia given the large number of differentials and the degree of variability in presentation.² Myasthenia gravis should be suspected if there are variable cover test measurements (especially in direction, such as changing from exophoria to esophoria) or extraocular movements between visits. Suspicion should also be raised when testing is not consistent with a specific palsy or simple tropia. It is often these cases presenting with diplopia alone where myasthenia is not suspected until the follow up visit when the data seems to contradict notes from the previous visit. In exceedingly rare cases, complete external ophthalmoplegia may be the presenting symptom of myasthenia gravis.²

Ptosis and Diplopia

About half of patients with myasthenia gravis will present with both ptosis and diplopia as their first symptoms. Cranial nerve 3 palsy can be a common misdiagnosis with these findings.^2,3 Testing of eyelid, pupil, and extraocular muscle function should be carefully performed.

A third-nerve palsy presents with ptosis (86%) of a severe degree due to paralysis of the levator palpebrae superioris. Pupil dysfunction (43%) may also occur, resulting in mydriasis and poor reaction to light. A third-nerve palsy will result in diplopia (when the ptotic lid is lifted out of the visual axis) and will have cover test results consistent with a palsy of one or several of the following extraocular muscles: inferior rectus, superior rectus, medial rectus, and inferior oblique.⁶

Conversely, myasthenia gravis may present with varying degrees of ptosis, ranging from mild to severe. The clinician can be less suspicious of a third-nerve palsy in cases that present with a milder degree of ptosis. However, in cases with a more dramatic ptosis and diplopia that is not consistent with a third-nerve palsy, clinical testing (such as ice pack test or forced eyelid closure test) can be performed quickly and reliably in the office. A ptosis from a third-nerve palsy will not change with any testing in office, whereas ptosis from myasthenia gravis may improve temporarily with these tests. Myasthenia gravis will never affect the pupillary fibers given it is a disease of skeletal muscle and not smooth muscle (such as the iris dilator and sphincter). However, the presence of a normal pupil cannot rule out a third cranial nerve palsy.

DIAGNOSIS

Diagnosis – Serologic Testing

Autoantibodies for acetylcholine receptors account for approximately 80% of cases.² Similar numbers were found in a study comparing anti-AChR seropositivity between generalized myasthenia gravis (GMG) and ocular myasthenia gravis (OMG) found 88% seropositivity in GMG and 73% seropositivity in OMG.³ Muscle-specific kinase antibodies have reported to comprise 4-6% of myasthenia gravis cases. Low-density lipoprotein 4 (LPR4) antibodies are the most recent to be discovered and are reported to be prevalent in approximately 2% of cases. In 5-10% of cases, no autoantibodies can be found and this is referred to as seronegative myasthenia gravis.^1,7 It is important to note that historically, this percentage was higher but has reduced with improved methods of detecting known autoantibodies has and with the discovery of new antigenic targets. Perhaps other autoantibodies exist, or current methods of detection are not sensitive enough in certain cases.

Diagnosis – Clinical Testing

Ptosis with or without diplopia:

Clinical testing for myasthenia gravis in cases presenting with ptosis includes three highly accurate and readily available tests, all of which can be performed at the initial examination.

1. Cogan’s Lid Twitch: the patient gazes downwards for fifteen seconds then quickly returns to primary gaze. If positive, there will be a brief overshoot upwards of the ptotic lid before slowly falling to the original ptotic positioning. This test has a reported sensitivity of 75% and specificity of 99%.²
2. Ice Pack Test: an ice pack is placed over the ptotic eye for two minutes. A positive result is an increase in eyelid positioning of >2 mm. This test has a sensitivity of 94% and specificity of 97%,.¹
3. Forced Eyelid Closure Test: the patient squeezes their eyes shut for a minimum of ten seconds and then quickly opens and fixates in primary gaze. A positive result is a brief excessive overshoot of the affected eyelid that then gradually falls to its original ptotic positioning. This test has a reported sensitivity of 94% and specificity of 91%.⁸

Diplopia without ptosis:

Cases that present as diplopia in isolation are more challenging to diagnose. Myasthenia gravis is often missed at the initial examination if findings are consistent with a phoria, tropia, or cranial nerve palsy. It is common that diplopia-exclusive cases are diagnosed upon follow-up visits when findings are not consistent, or even completely opposite, than those found at the initial examination. Myasthenia gravis should be considered in cases where the diplopia testing is not consistent with a simple tropia or palsy, or where the results have fluctuated in magnitude or direction over multiple visits.

Some sources mention performing the ice pack test in those with suspected myasthenic diplopia. A positive result is an improvement in ocular deviation of at least 50%, or by 10 prism diopters or more for deviations larger than 20 prism diopters, after five minutes of applying the ice pack. The use of the ice pack test in suspected myasthenic diplopia cases still has a remarkably high specificity (92.3-98.6%), as with myasthenic ptosis cases, but is much less sensitive (74-76.9%).^1,9

TREATMENT

Acetylcholinesterase Therapy

Most treatment options available are indicated for generalized myasthenia gravis and are not specific to ocular myasthenia gravis. Anticholinesterase drugs, such as pyridostigmine, work at the neuromuscular junction to increase the availability of acetylcholine and are the most common form of first-line treatment. This medication appears to only be effective at symptomatic relief in 20-40% of ocular myasthenia gravis patients.¹ Additionally, anticholinesterase drugs do not prevent progression to myasthenia and only work on improving symptoms. Cholinergic side effects, such as increased salivation and diarrhea, are common with this medication.

Non-Specific Immunosuppressive Agents

Corticosteroids can be an effective treatment for myasthenia gravis. This class of medication works on the inflammatory process by decreasing CD4+ T-cell activation and anti-AChR antibody synthesis. Corticosteroids are started at a higher daily dosage at initial diagnosis for immediate symptom relief, and then moved to an alternating day dosage for long-term management to reduce the potential for side effects. Unfortunately, there is not a consensus in the literature on the appropriate dosage and length of dosage for corticosteroid treatment. However, there are trials that show 29% of patients with ocular myasthenia gravis remained dependent on corticosteroids for long term management.¹⁰ Some retrospective case studies have suggested steroids can reduce the rate of conversion from OMG to GMG, however, these were non-randomized and have not further been investigated or supported.¹¹

Azathioprine can also be an effective treatment for MG patients, which is often dosed either independently or concurrently with prednisone. This class of medication works on T and B cell proliferation and typically requires months of treatment before clinical improvement is evident. Specifically with OMG, it is often prescribed concurrently with prednisone, as studies have shown a slightly higher rate of improvement in symptoms with the combination.¹⁰ Cyclosporine is an additional immunosuppressant that is prescribed when patients are resistant to other therapies. Cyclosporine inhibits T-cell function, specifically Th1 and Th2 cytokine production, and it can show improvement in symptoms after only a few weeks of treatment. In general, immunosuppressive agents have not shown to reduce the conversion of OMG to GMG.³

Targeted Immunosuppressive Agents

Two major intravenous complement inhibitors have recently been released for the treatment of anti-AChR antibody-positive generalized myasthenia gravis: eculizumab and ravulizumab. However, trials of ocular myasthenia gravis have yet to be performed for these treatment options. Current clinical trials suggest an overall improvement in quality of life through the duration of treatment, which includes improvement in eyelid drooping and diplopia, but the reported results do not specifically separate ocular involvement or symptoms. The role of these medications in ocular myasthenia gravis is unclear at this time.^12,13

Efgartigimod, a human IgG1 antibody Fc fragment, has recently been released as intravenous treatment in cases of generalized myasthenia gravis, regardless of anti-acetylcholine receptor antibody status. In randomized controlled studies, there appears to be some promise in being a well-tolerated treatment that can improve quality of life, though its role in ocular myasthenia gravis is yet to be explored.¹⁴

Thymectomy

Thymectomy, or surgical removal of the thymus gland, is a common therapy in myasthenia gravis cases associated with thymic abnormalities, such as thymoma (10-15%) and follicular hyperplasia (60-65%). It is thought that the hyperplastic thymus is the site of immunization against acetylcholine receptors and the production of anti-AChR antibodies. The pathogenic role of thymoma is unclear in the disease. Despite an absence of randomized controlled studies, thymectomy continues to be a mainstay therapy for cases of generalized myasthenia gravis in the setting of thymic abnormalities. Thymectomy has been demonstrated to have clinical improvement in 70-80% of patients. However, its role in patients with OMG is highly controversial and it should not be considered as the initial treatment option, even in the presence of a thymoma. The results of thymectomy in OMG vary greatly within the literature and remission rates are highly dependent on the definition of remission in each study. Some argue that thymectomy should continue to be considered in patients with OMG that have a high risk of converting to GMG or those who are resistant to immunosuppressive and anticholinesterase therapies, yet there is no evidence to support this. Ultimately, a lack of consensus remains on the definition of remission in these patients, as well as an absence of randomized controlled trials investigating the long-term efficacy of thymectomy for OMG.^10,15-17

CONCLUSION

Myasthenia gravis is often a challenging diagnosis – yet sometimes the most challenging aspect is simply considering the condition. Often, the disease will mimic other more common conditions, leading clinicians to consider more likely differentials first. It is essential that clinicians remember the hallmark of myasthenia gravis is fatigability and variability and consider myasthenia gravis if the case history is suggestive of these patterns. Most patients with myasthenia gravis will have ocular symptoms throughout the course of their disease, but even more impressively, ocular symptoms are the initial presentation in nearly half of the cases. Therefore, eye care providers are often responsible for ordering testing and referring patients to appropriate specialists in a timely manner to improve symptoms. Fortunately, several clinical tests with high sensitivity and specificity are easy to perform in-office at the initial examination. If positive, there is a high likelihood of myasthenia gravis and appropriate referrals can be made accordingly. Effective treatment options exist and continue to become more specific to myasthenia gravis, though no treatments exist solely for ocular myasthenia.

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Janessa Visin, OD, ABCMO

Kansas City VAMC | Kansas City, MO

Janessa Visin, OD graduated from the University of Missouri-St. Louis with honors and completed her residency in Ocular Disease, Glaucoma, and Low Vision at the Kansas City VAMC, where she currently is practicing full time. She enjoys writing in optometry and is currently the Chief Medical Editor for KMK Optometry Boards Review, as well as an editor for JoMO.

Elizabeth Phillips, OD

Kansas City VA Medical Center | Kansas City, MO

Dr. Elizabeth Phillips graduated from UMSL College of Optometry in 2016. The following year she completed her ocular disease and low vision residency at the Kansas City VA Medical Center, where she currently works, teaching students and residents. She is board certified in medical optometry (ABCMO) and is pursuing her fellowship with AAO this fall.