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Alleviating Variable Diplopia with Monovision Contact Lenses in a Patient with Multiple Sclerosis and Myasthenia Gravis Shelly E

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Alleviating Variable Diplopia with Monovision Contact Lenses in a Patient with Multiple Sclerosis and Myasthenia Gravis Shelly E Title: Double Trouble: Alleviating Variable Diplopia with Monovision Contact Lenses in A Patient with Multiple Sclerosis and Myasthenia Gravis Shelly E. Lomax, OD and JulieAnne M. Roper, OD, MS Abstract Symptoms of diplopia and ptosis in a patient with multiple sclerosis lead to the rare concurrent diagnosis of myasthenia gravis. When traditional treatments are unsuccessful in alleviating incomitant diplopia, monovision contact lenses should be considered. I. Case History Demographics 69-year-old Caucasian male Chief complaint Double vision with horizontal, vertical, and torsional components Ocular history Diplopia Ptosis Pertinent medical history Myasthenia Gravis (MG) Multiple Sclerosis (MS) Medications Pyridostigmine bromide Avonex Other salient information Right side progressive muscle weakness with very limited movement Dependent upon wheelchair II. Pertinent findings Clinical EOMs: FROM OU, lagging movement OS Habitual Rx: +1.75-0.50x080 OD, +1.50-1.00x088 OS, +2.50 add OU Cover test in primary gaze: 8-10^LH, 6^RET at distance, 6^LH, 4 XP at near (variable) Alternating XT at near 1 month prior Cover test in 9 positions of gaze: incomitant deviation Von Graefe: 8-10^LH, 6^RET at distance, 6^LH, 4 XP at near (variable) 4^RH at distance 1 month prior Physical Ptosis OD>OS Right side muscle weakness Wheelchair dependent Laboratory studies Positive blood test for Acetylcholine receptor binding, blocking, and modulating antibodies. Radiology studies MRI: Multiplanar images of the brain, including T1 weighted post gadolinium contrast images revealed multiple focal areas of abnormal signal intensity at the deep white matter of the periventricular regions bilaterally. The number and size of the lesions increased from the MRI brain scan 7 years prior. Several similar appearing focal areas of abnormal signal intensity had developed in the pons and medulla of the brainstem as well as in the deep white matter of both cerebellar hemispheres since the previous MRI brain scan. These findings are radiographically consistent with the clinical diagnosis of MS. Electrodiagnostic testing Single-fiber electromyography of the left facial nerve/frontalis shows greater than 10% decrement post exercise consistent with a disorder of the neuromuscular junction as in MG. III. Differential diagnosis Primary Transient diplopia secondary to MG and MS Others Decompensated phoria Convergence or divergence insufficiency Spasm of accommodation or convergence Ischemia of extraocular muscles TIAs involving the vertebrobasilar system Superior oblique myokymia Ocular neuromyotonia Cyclic esotropia Skew deviation IV. Diagnosis and discussion A newly noted ptosis and variable diplopia in our patient with MS warranted further serological and electrodiagnostic testing that revealed a concurrent diagnosis of MG. Despite systemic treatment by neurology, the patient was plagued by persistent diplopia. o Cover test findings in 9 positions of gaze revealed an incomitant deviation of varying magnitude and direction over several visits. o Due to the variable deviation, alignment was unable to be achieved with prism. Patching had relieved symptoms for several months until the patient became intolerant due to irritation. o The patient was reconsulted to neurology for consideration of medication adjustment, but neurology deferred increasing the pyridostigmine. The patient’s awareness of suppression to reduce symptoms of double vision prompted fitting with contact lenses in a monovision modality. o The dissociation properties of the monovision lenses were able to completely alleviate the patient’s diplopia symptoms. o Despite the patient’s physical limitations of severe right side muscle weakness, the patient was able to perform insertion and removal of soft contact lenses. V. Treatment, management Treatment The dual diagnosis of MS and MG is not only rare and unfortunate, but can also lead to ocular manifestations that can be challenging to manage. The literature discusses treatment options for the variable diplopia that can be associated with MG including oral medications, surgery, and prism. o However, our patient became intolerant to all historically standard treatment options. o There are documented cases of relieving diplopia by means of disparity such as in monovision contact lenses, including one case report of a patient with a significant vertical imbalance. We decided to apply this concept to our patient’s incomitant diplopia as a new, unique treatment for ocular MG that would eliminate the need for patching. o This less traditional option of monovision contact lenses proved to be the only viable option for our patient and successfully alleviated our patient’s symptoms. Bibliography As MG typically presents with ocular symptoms, the optometrist can play an important role in diagnosis and management of these patients. 18+ articles on MG diagnosis, treatment, and management, including: 1. Karmel, M. Deciphering diplopia. Eyenet. November/December 2009: 31-34. 2. Nair AG, Patil-chhablani P, Venkatramani DV, Gandhi RA. Ocular myasthenia gravis: a review. Indian J Ophthalmol. 2014;62(10):985-91. 3. López-Cano M, Ponseti-Bosch JM, Espin-Basany E, Sánchez-García JL, Armengol- Carrasco M. Clinical and pathologic predictors of outcome in thymoma-associated myasthenia gravis. Ann Thorac Surg. 2003 Nov; 76(5):1643-9; discussion 1649. 4. Miller N. Walsh and Hoyt's Clinical Neuro-Ophthalmology. 4th ed. Baltimore, Md: Williams & Wilkins;1969;1 :280-281. 5. March GA, Johnson LN. Ocular myasthenia gravis. J Natl Med Assoc. 1993;85(9):681-4. 6. Springhouse (Editor). Professional Guide to Pathophysiology. 3rd ed. Lippincott Williams & Wilkins; 2010;8:297. 7. Haines SR, Thurtell MJ. Treatment of ocular myasthenia gravis. Curr Treat Options Neurol. 2012;14(1):103-12. 8. Kupersmith MJ. Ocular myasthenia gravis: treatment successes and failures in patients with long-term follow-up. J Neurol 2009;256:1314–20. 9. Grob D, Arsura EL, Brunner NG, Namba T. The course of myasthenia gravis and therapies affecting outcome. Ann N Y Acad Sci. 1987;505:472–99. 10. Sommer N, Melms A, Weller M, Dichgans J. Ocular myasthenia gravis. A critical review of clinical and pathophysiological aspects. Doc Ophthalmol. 1993;84(4):309-33. 11. Grigg J. Extraocular muscles: Relationship of structure and function to disease. Aust N Z J Ophthalmol. 1999;27:369–70. 12. Benatar M. A systematic review of diagnostic studies in myasthenia gravis. Neuromuscul Disord. 2006;16(7):459-67. 13. Odel JG, Winterkorn JM, Behrens MM. The sleep test for myasthenia gravis. A safe alternative to Tensilon. J Clin Neuroophthalmol. 1991; 11:288-292. 14. Oosterhuis HJ. The ocular signs and symptoms of myasthenia gravis. Doc Ophthalmol. 1982;52(3-4):363-78. 15. Roh HS, Lee SY, Yoon JS. Comparison of clinical manifestations between patients with ocular myasthenia gravis and generalized myasthenia gravis. Korean J Ophthalmol. 2011;25(1):1-7. 16. Glaser JS. Neuro-Ophthalmology. 2nd ed. Philadelphia, Pa: JB Lippincott Co; 1990:392- 398. 17. Kupersmith MJ. Does early treatment of ocular myasthenia gravis with prednisone reduce progression to generalized disease? J Neurol Sci 2004;217:123-4. 18. Kupersmith MJ, Ying G. Ocular motor dysfunction and ptosis in ocular myasthenia gravis: effects of treatment. Br J Ophthalmol 2005;89:1330-4. VI. Conclusion Clinical pearls The possibility of dual systemic disease processes causing ocular complications should not be neglected, and further testing should be done when a second disease process with potentially serious complications is suspected. As in our case, MG should be considered in patients with MS who have fatigue, diplopia, or ptosis. Instead of traditional patching, monovision contact lenses to alleviate incomitant diplopia may be considered as a unique treatment option for patients with MG and MS. .
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