Abstract

Myasthenia gravis (MG) is an autoimmune disease in the neuromuscular junction. This is a relatively uncommon disorder characterized by fluctuating muscle weakness, worst with exertion and improves with rest. This disease is treatable but can result in significant morbidity and mortality. The etiology of MG is commonly acquired autoimmune but, in some case, result from genetic abnormalities in the neuromuscular junction.1 The incidence of MG is about 4.1-30 points million per year, and the prevalence rate ranges from 150-200 cases per million.2 It is believed that MG incidence has increased worldwide over the past seven decades. The majority of MG was estimated at 1 in 200,000 from 1915 to 1934, grew to 1 per 20,000 after the introduction of anticholinesterase drugs in 1934, and rose to 1 per 17,000 population after the discovery of AChR antibodies in 1969.3 Sex and age appear to influence the occurrence of myasthenia gravis. Below 40 years of age, the female: male ratio is about 3: 1; however, between 40 and 50 years, as well as during puberty, it is roughly equal. Over 50 years, it occurs more commonly in males.3
 Cognitive impairment in patients with myasthenia gravis is still a matter of debate. There is some evidence that central nervous system involvement in myasthenia gravis contributes to cognitive impairment—nearly 60% of individuals with MG report memory difficulties.4 Mao et al. reported in their metanalysis study that patients with suspected MG performed worse than healthy controls regarding verbal learning and memory.5 Research by Klaus et al., 2022 on myasthenia gravis showed structural and functional changes in the patient's brain. Structural changes were seen in the form of a significant decrease in the volume of gray matter in the cingulate gyrus, inferior parietal lobe, and fusiform gyrus. Functional changes are characterized by decreased performance in cognitive function, working memory, and somatosensory-related spatial orientation.6

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