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Myasthenia Gravis
Published in Charles Theisler, Adjuvant Medical Care, 2023
The term myasthenia gravis literally means “grave or serious muscle weakness.” Myasthenia gravis is an autoimmune disorder in which the body's own antibodies block the transmission of nerve impulses to muscles, causing varying degrees of voluntary muscle weakness and muscles that tire easily. The muscles that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are most often involved in the disorder.1 A variable combination of legs, arms, or respiratory weakness can also occur. Myasthenia gravis in 15%-20% of cases can cause respiratory failure, which can be fatal and requires immediate emergency medical care.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Myasthenia gravis is caused by the autoimmune destruction of ACh receptors. ACh produced at the synapse is broken down by AChE before the patient’s muscles have contracted. By blocking AChE, the breakdown of ACh is prevented, and the muscle is stimulated until it contracts. Drugs that block AChE are called acetylcholinesterase inhibitors, for example, pyridostigmine, and are the mainstay of myasthenia gravis management.
Beginnings
Published in Peter Tate, Francesca Frame, Bedside Matters, 2020
Nearly three years went by and, by some fluke or misjudgment on Newcastle University's part, I started there on 2nd September 1963, my 17th birthday. I had been away at boarding school, but once back at home it was obvious that Dad was increasingly unwell but pig-headedly soldiering on; his friend had told him he was ok so he would get through it. We persuaded him to go back, Henry was unsure and sent him for a second opinion from his deputy and rapidly rising star John Walton. After a couple of tests and a brief admission the diagnosis of myasthenia gravis was made. I think Henry was mortified. I do know that in my entire time at university he never spoke to me once, claiming later that he did not know I was Ivan's son. He did you know.
Ophthalmic complications of immune checkpoint inhibitors
Published in Orbit, 2022
Edward J. Wladis, Madhavi L. Kambam
Autoimmune phenomena are also associated with immune checkpoint inhibitors, and this finding may result from the restoration of an enhanced immune response that correlates with the mechanism of action of this class of medications. Lorenzo et al noted the development of a myasthenic crisis in a 67-year-old male who received two doses of pembrolizumab for mesothelioma. The patient presented with diplopia and left upper eyelid ptosis, and serologic evaluation identified the presence of acetylcholine receptor antibodies. Unfortunately, the patient’s disease was refractory to corticosteroids, pyridostigmine, and intravenous immunoglobulin.22 Jeyakumar et al documented a case of new-onset myasthenia gravis that was associated with myocarditis and myositis after cemiplimab therapy.23 While the ophthalmic findings of the presentation are somewhat limited, the authors note that the patient suffered from the acute onset of blurred vision. These reports are consistent with several previous findings of myasthenia gravis in this clinical setting.24
Serum Biomarkers in Neuro-Ophthalmology: When to Test
Published in Seminars in Ophthalmology, 2021
Devon A. Cohen, Ryan Gise, Eric D. Gaier
Myasthenia gravis causes fatigable weakness due to an autoimmune disruption of neuromuscular synaptic transmission. Approximately 40% of patients diagnosed with myasthenia gravis present with ocular symptoms including diplopia and ophthalmic signs including fatigable ptosis, Cogan’s lid twitch, and pupil-sparing ophthalmoplegia.7 Of these, approximately 38% of cases remain ocular. The mechanism of antibodies targeting the muscle-specific nicotinic acetylcholine receptor (the post-synaptic receptor required for synaptic transmission at the neuromuscular junction) was uncovered by Patrick and Lindstrom in 1973.8 Despite a clear pathogenic link, acetylcholine receptor (AChR) antibodies are only detectable in about 50% of patients with ocular myasthenia gravis. Muscle-specific kinase (MuSK), a tyrosine kinase required for formation and maintenance of the neuromuscular junction, was identified as another marker of MG, and according to a retrospective study of 82 patients seropositive for MuSK, only 3 (3.7%) of the patients presented with isolated ocular myasthenia gravis.9 Among patients with generalized myasthenia gravis, AChR antibodies are positive in about 80% of patients, and MuSK antibodies are positive in 10%.9–12
Corneal melting in a case undergoing treatment with pembrolizumab
Published in Clinical and Experimental Optometry, 2020
Chang‐chi Weng, Chih‐chiau Wu, Pei‐yu Lin
A 31‐year‐old Asian woman with metastatic thymoma complicated with myasthenia gravis was referred for ophthalmic evaluation due to symptoms of bilateral red eyes, pain with foreign body sensation, photophobia, and blurred vision. She had right side pleural seeding and bone metastasis, without ocular or adnexal involvement. The symptoms of myasthenia gravis were well‐controlled with oral methylprednisolone and pyridostigmine. Since then she had no ptosis and could blink normally. Seventeen days before referral, she was treated with the first cycle of pembrolizumab (2-mg/kg) because of tumour progression after chemotherapy, including etoposide, cisplatin, and combining radiotherapy in the past two years. She received the last course of chemotherapy as etoposide and cisplatin five months before the first cycle of pembrolizumab and had no prior history of dry eye syndrome or ocular surface disease.