Ocular myasthenia gravis: case report

Abstract

Background. Myasthenia gravis (MG) is an autoimmune disease in which the patients’ immune system, through the antibodies, attack the nicotinic acetylcholine receptors located on the postsynaptic neuro-muscular junction, resulting in fatigability and weakness of skeletal muscles. If weakness is limited only to the extrinsic ocular muscles and to the levator palpebrae superioris, the disease is called Ocular MG. However, ocular muscle weakness can be a debut symptom in the Generalized form of the MG (GMG) as well. Thus, the surveillance of the patient in early stage is essential, particularly during first 2 years, as most of them develop GMG within this period. Case report. A 52-year-old man was admitted at the Neurology Department with weakness in the upper eyelids, expressed through the reduction of the palpebral fissures, gradually through the first half of the day (blepharoptosis), incapacity to fully open the eyes, moderate diffuse headache, anxiety and difficulty in falling asleep. He presented similar symptoms for about 15 years. In 2009, the patient did an electroneurography of the median nerve, where a positive decrement was registered and the diagnosis of Ocular Myasthenia Gravis was first mentioned. The patient was given treatment with Ipidacrinum, with no positive dynamics. After almost 10 years, in 2017, the patient’s general condition worsened, he was not capable anymore of driving, his quality of life has decreased and he addressed the neurologist again. He is tested on the serum antibodies. Both the Anti-acetylcholine receptor (anti-AchR) antibodies and the Anti-muscle-specific tyrosine kinase (anti-MuSK) antibodies were found slightly positive (AchR Ab – 0.25 [normal value <0.2&#93;; MuSK Ab – 0.05 [normal value <0.05&#93;). After several months, the anti-AchR Ab raised up to 0.52nmol/L. The Tensilon (Neostigmine) test was performed and revealed only a week positive outcome: after administrating 1ml Neostigmine i/m, the palpebral fissures measured 4 mm, compared to 3 mm before the injection. Based on these borderline results, we confirmed the Ocular Myasthenia Gravis form as diagnosis and we added Prednisolone to the treatment, with moderate improvement of the symptoms.Conclusions. Based on the described evidence, the increase in the concentration of the antibodies against acetylcholine receptors correlate with the development of Myasthenia gravis. The worsening of the patient’s symptoms may be associated with inefficient plan of treatment. Being symptomatic despite the treatment with a cholinesterase inhibitor (Neuromedin) demands adding a glucocorticoid drug (ex. Prednisolone).