Introduction

Myasthenia gravis (MG) is a chronic neuromuscular condition caused by an autoimmune process that mostly affects the voluntary muscles. It is characterized by fatigue and weakness in the muscles. Autoantibodies directed against acetylcholine receptors (AChR) or, less frequently, muscle-specific kinase (MuSK) or other proteins involved in neuromuscular transmission, are the root cause of it.¹ Muscle weakness of varied degrees is a common symptom of MG, which is frequently made better by rest and made worse by physical exercise.

Epidemiology

Although MG affects people of all ages and races, it is more common in males over 60 and women under 40.² Prevalence rates range from 15 to 179 instances per million, with an estimated incidence of 3 to 30 cases per million annually.³ Geographic variations may exist, though.

Pathophysiology

Autoantibodies against important proteins involved in signal transduction at the neuromuscular junction cause neuromuscular transmission to be impaired, which is the defining feature of myasthenia gravis (MG). These autoantibodies often target the AChR, which results in its destruction and a decrease in the quantity of functioning AChRs on the postsynaptic membrane.⁴ This leads to the decrease in neuromuscular transmission, which in turn produces exhaustion and muscle weakness.

Clinical presentation

A wide range of symptoms, from minor eye symptoms to severe generalized weakness involving respiratory muscles, can manifest clinically as MG. Ocular symptoms, which affect about half of all MG patients, include ptosis and diplopia, which are common first presentations.⁵ Often, this is followed by a generalized weakness that affects the muscles used for speaking, chewing, swallowing, and limb movement. A potentially fatal consequence known as respiratory failure might result from weakening of the breathing muscles.

Diagnosis

Clinical evaluation, serological testing for autoantibodies (e.g anti-AChR, anti-MuSK), electrophysiological studies (e.g nerve conduction studies, electromyography), and pharmacological tests (e.g edrophonium or neostigmine test) are all used in the diagnosis of myasthenia gravis syndrome (MG).⁶ Since thymoma is linked to MG in a small percentage of individuals, imaging tests like CT or MRI may be helpful in evaluating thymic abnormalities.

Treatment

Enhancing neuromuscular transmission, reducing symptoms, and preventing aggravating of the disease are the goals of MG care. Acetylcholinesterase inhibitors, such as pyridostigmine, immunosuppressive drugs, such as corticosteroids, azathioprine, and mycophenolate, and immunomodulatory therapy, such as intravenous immunoglobulin and plasma exchange, are available as treatment options.⁷ People with generalized MG or thymoma may be candidates for thymectomy, particularly if they are younger people.

Prognosis

The intensity of symptoms, age of onset, presence or absence of thymic disease, and responsiveness to treatment all affect the prognosis of MG. Many patients have symptomatic relief and stable illness control with the right care. But MG can cause a considerable amount of morbidity and death, especially when respiratory muscle weakness and myasthenic crisis occur.

Conclusion

Due to decreased neuromuscular transmission, myasthenia gravis is a complicated autoimmune condition that causes fatigue and muscle weakness. Even though knowledge and treatment of MG have advanced significantly, more study is still required to fully understand the disease's pathophysiology, enhance diagnostic techniques, and provide tailored treatments that will benefit those who are affected.