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Myasthenia gravis (MG) is an autoimmune disease that affects the voluntary skeletal muscles. It is characterized by transient weakness of the muscles that improves with rest. Muscle weakness involving the eyes can produce signs or symptoms of diplopia, blurred vision, ptosis, and ophthalmoplegia. Ptosis is defined as an abnormal eyelid "drooping" beyond the normal 1 to 2 mm of the upper limbus of the cornea. Hence, most patients with MG have ophthalmic manifestations. Among all patients with MG, up to half will have exclusively ocular symptoms. In these cases, the condition is referred to as ocular myasthenia. CASE
A 60-year-old man was referred from a neurology clinic for management of intermittent diplopia for greater than 1 year and intermittent bilateral ptosis for the prior year. He reported that he first noticed symptoms of MG at the age of 42, but did not receive the diagnosis until 1 year before his aforementioned neurology examination. He was prescribed spectacles with bilateral ptosis crutches. A diagnosis of severe seronegative MG was subsequently confirmed with neurologic examination and antibody testing.
Because patients with undiagnosed myasthenia gravis may present initially with ocular signs or symptoms, it is important for the optometrist to be familiar with the condition and the simple "in-office" tests that can be performed to establish a tentative diagnosis and management plan. The optometrist can also participate in the management of ocular manifestations of myasthenia and should be familiar with the use of a ptosis crutch (in addition to prism spectacles or occlusion therapies if indicated) as a nonsurgical intervention for ptosis.
Minneapolis Veterans Affairs Medical Center, Minneapolis, Minnesota; University of Missouri-Saint Louis College of Optometry, Saint Louis, Missouri.
This article was published in the following journal.
Name: Optometry (St. Louis, Mo.)
Myasthenia gravis is a chronic, autoimmune, neuromuscular disease characterized by fluctuating weakness of voluntary muscle groups. Although genetic factors are known to play a role in this neuroimmun...
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A disorder of neuromuscular transmission that occurs in a minority of newborns born to women with myasthenia gravis. Clinical features are usually present at birth or develop in the first 3 days of life and consist of hypotonia and impaired respiratory, suck, and swallowing abilities. This condition is associated with the passive transfer of acetylcholine receptor antibodies through the placenta. In the majority of infants the myasthenic weakness resolves (i.e., transient neonatal myasthenia gravis) although this disorder may rarely continue beyond the neonatal period (i.e., persistent neonatal myasthenia gravis). (From Menkes, Textbook of Child Neurology, 5th ed, p823; Neurology 1997 Jan;48(1):50-4)
Any autoimmune animal disease model used in the study of MYASTHENIA GRAVIS. Injection with purified neuromuscular junction acetylcholine receptor (AChR) (see RECEPTORS, CHOLINERGIC) components results in a myasthenic syndrome that has acute and chronic phases. The motor endplate pathology, loss of acetylcholine receptors, presence of circulating anti-AChR antibodies, and electrophysiologic changes make this condition virtually identical to human myasthenia gravis. Passive transfer of AChR antibodies or lymphocytes from afflicted animals to normals induces passive transfer experimental autoimmune myasthenia gravis. (From Joynt, Clinical Neurology, 1997, Ch 54, p3)
Experimental animal models for human AUTOIMMUNE DISEASES OF THE NERVOUS SYSTEM. They include GUILLAIN-BARRE SYNDROME (see NEURITIS, AUTOIMMUNE, EXPERIMENTAL); MYASTHENIA GRAVIS (see MYASTHENIA GRAVIS, AUTOIMMUNE, EXPERIMENTAL); and MULTIPLE SCLEROSIS (see ENCEPHALOMYELITIS, AUTOIMMUNE, EXPERIMENTAL).
A rapid-onset, short-acting cholinesterase inhibitor used in cardiac arrhythmias and in the diagnosis of myasthenia gravis. It has also been used as an antidote to curare principles.
A cholinesterase inhibitor with a slightly longer duration of action than NEOSTIGMINE. It is used in the treatment of myasthenia gravis and to reverse the actions of muscle relaxants.
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